Relationship of Different Hormone levelsand Effect of six-month Cholecalciferol Supplementationin Sarcopenic End-Stage Kidney Disease: A prospective interventional study | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Relationship of Different Hormone levelsand Effect of six-month Cholecalciferol Supplementationin Sarcopenic End-Stage Kidney Disease: A prospective interventional study DISHA ARORA, LALIT PURSNANI, Himansu Mahapatra, MUTHUKUMAR BALAKRISHNAN, and 7 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7434137/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 7 You are reading this latest preprint version Abstract Background: Hormonal relationship especially effect of long-term vitamin D supplementation to sarcopenic patients is understudied. This study investigatedassociated risk factors and correlation of different hormones with sarcopenia. Further, effects of six-month cholecalciferol supplementation and quality of life were also studied. Methodology : CKD5 patients aged 18–60 years were screened for sarcopenia using handgrip strength and bioimpedance-based muscle mass. Sarcopenia was classified as probable, confirmed, and severe categories. Confirmed sarcopenic cases were supplemented with 60,000 IU weekly cholecalciferol for 12 weeks in vitamin D deficit and fortnightly for 6 weeks in sufficient patients. Comprehensive nine hormonal profile and risk factor assessment in all sarcopenic patients were done. All were subjected for QoL by KDQOL-36 SF at baseline and 6 months. Changes in Sarcopenia, physical and mental domains of QoL (PCS and MCS) were studied at baseline and 6 th month. R esults : Of 401 patients, sarcopenia prevalence as probable, confirmed and severe were 333 (82.29%), 134(33.4%) and 124(25.44%) respectively with higher prevalence in dialysis patients.Vitamin D supplementation showed improvement in confirmed and severe sarcopenia at 3 rd month (13.1 %.and 41.1%) and 6 th month (23/3% and 66.9%) respectively (p = 0.001). Vitamin D levels deficiency significantly reduced from 80.6% at baseline to 45.5% after supplementation.At six months among non-responder sarcopenic patients exhibited greaterbaseline hormonal abnormalities like high insulin resistance, hyperprolactinemia, lower T3 levels, whereas responder had better baseline muscle strength/mass and higher vitamin D levels. Among non-responder who were still vitamin D deficient showed positive correlation of vitamin D deficiency with IGF-1, testosterone deficiency and negative correlation with insulin resistance was seen. Overall, IGF-1deficiency, insulin resistance,subclinical hypothyroidism, hypogonadism, hyperprolactinemia, were highly prevalent in sarcopenic patients. KDQOL-36 scores improved significantly in mean PCS(p=0.004) and MCS (p = 0.003) after vitamin D supplementation. Diabetes and vitamin D deficiency were determined as risk factor of sarcopenia. Conclusion : Diabetes and vitamin D deficiency are risk factor for sarcopenic CKD5 patients. Six months vitamin D supplementation improved sarcopenia and quality of life in them. Non responsive sarcopenic patients had hormonal imbalances which remain uncorrected or may have blunted therapeutic effects of vitamin D. Trial registration: CTRI/2025/08/092512 – dated 6 th august 2025 (retrospectively registered) Uremic sarcopenia hormonal relation cholecalciferol supplementation chronic kidney disease quality of life Figures Figure 1 Figure 2 Background Sarcopenia, marked by the progressive loss of muscle mass, strength, and function, is a frequent but underrecognized complication of chronic kidney disease CKD. Although, exact prevalence in different stages of CKD is understudied, existing literature showed it is prevalent as 5.9–28.7% of patients with stage 5 CKD not on dialysis and nearly 25.9–34.6%of those on dialysis( 1 ). Beyond its association with frailty and higher mortality, sarcopenia significantly impairs quality of life (QoL) by limiting physical performance and increasing hospitalization risk. Despite these consequences, routine screening remains limited, particularly in resource-constrained settings where body mass index (BMI) and fluid overload obscure muscle loss. Conventional tools such as DEXA scan are affected by fluid status, CT and MRI are costly, while bioelectrical impedance analysis (BIA), though feasible, lacks CKD-specific validation, underscoring the need for simple bedside tools for early diagnosis ( 2 ). Unlike age-related sarcopenia, uremic sarcopenia develops early due to inflammation, uremic toxins, protein-energy wasting, and endocrine dysfunction. An imbalance between anabolic hormones (IGF-1, testosterone, oestrogen, thyroid) and catabolic mediators (cortisol, PTH) drives muscle degradation. Further, vitamin D deficiency, nearly universal in CKD,worsens muscle health by impairing VDR-mediated pathways controlling protein synthesis, mitochondrial activity, and myogenesis( 3 ). Clinical trials of cholecalciferol for sarcopenia in CKD showed inconsistent outcomes, largely due to variability in CKD stage, dosing, formulations, baseline vitamin D status, and assessment methods( 4 – 6 ). Vitamin D also modulates multiple hormonal axes, enhancing IGF-1, stimulating testosterone, improving insulin sensitivity, suppressing cortisol, reducing PTH, and stabilizing thyroid and prolactin levels, thereby preserving muscle integrity ( 7 ). Despite growing evidence of vitamin D’s influence on these pathways, its role in reversing sarcopenia remains poorly understood. Persistent anabolic resistance may blunt its therapeutic effects, highlighting the need for studies that integrate both functional and hormonal abnormalities. To address these gaps, our study examines the long-term effects of individualized cholecalciferol supplementation on muscle mass, strength, and QoL in sarcopenic CKD patients. By integrating detailed hormonal profiling, we aim to clarify how vitamin D interacts with endocrine pathways and identify predictors of treatment response. Methods Study Design and Duration This was a prospective, interventional study conducted over a six-month period in the Department of Nephrology at a tertiary care centre. Inclusion and Exclusion Criteria Patients aged 18 to 60 years with CKD stage 5, attending either nephrology outpatient services or undergoing maintenance haemodialysis in the dialysis unit, were enrolled after providing written informed consent. Patients were excluded if they were bedridden or unable to perform physical function assessments, had any active malignancy, HIV, tuberculosis, chronic liver disease, or were pregnant. Additional exclusions included the presence of implanted cardiac devices that contraindicated the use of bioimpedance analysis, any known endocrine abnormality apart from diabetes mellitus, and the intake of vitamin D supplements, calcium-based phosphate binders, or corticosteroids within three months prior to enrolment. Definitions Sarcopenia was defined using the AWGS 2019 consensus. Probable sarcopenia was diagnosed when grip strength was low (< 28 kg in men and < 18 kg in women). Confirmed sarcopenia required low grip strength along with low appendicular skeletal muscle index (ASMI < 7.0 kg/m² in men, < 5.7 kg/m² in women). Severe sarcopenia further included low gait speed (< 1.0 m/s)( 8 ). Body Mass Index (BMI) was categorized based on Asian standards: <18.5 as underweight, 18.5–22.9 as normal, 23–24.9 as overweight, 25–29.9 as obese class I, and ≥ 30 kg/m² as obese class II( 9 ). Mid-upper arm circumference (MUAC) was considered low at ≤ 28.6 cm in men and ≤ 27.5 cm in women. Triceps fat fold (TFF) define fat depletion was taken as < 10 mm in men and < 13 mm in women. Mid-arm muscle circumference (MAMC) was calculated as MUAC-3.1415 x TFF. Severe malnutrition was considered as MAMC < 19 cmin men and < 16 cm in women. Sample Size Calculation Sample size was based on the study by Wang et al., which examined the effects of oral cholecalciferol on sarcopenia in ESRD patients( 9 ). Using G*Power software with repeated measures ANOVA at three time points (baseline, 3 months, and 6 months), assuming an effect size of 0.5, significance level (α) of 0.05, and power of 90%, a minimum of 96 participants were required. With a 20% attrition adjustment, the target sample size was 116. Based on sarcopenia prevalence of 25–40% among CKD5 patients, approximately 300–480 patients were planned for screening. Further, for hormonal assessment, sample size was calculated for each of the nine hormones we used in the study and sample size ranged from minimum of 171 to maximum of 346 ( 10 – 12 ), however study remains underpowered for hormone analysis. Data Collection 1. Demographic and Clinical Examination Baseline data including age, sex, and known comorbidities (e.g., diabetes, hypertension, cardiovascular disease) were recorded. Aetiology of CKD was determined from clinical history or previous renal biopsy. For dialysis patients- access (AV fistula or catheter), frequency (2–3 sessions weekly), and dialysis vintage were documented. Anthropometric measurements included height, weight, BMI, MUAC, TFF, and MAMC. 2. Sarcopenia Diagnosis Handgrip strength was measured using a handheld dynamometer on the dominant or non-fistula arm, in a seated position with the elbow flexed at 90°. The average of three readings, spaced one minute apart was used. Patients with reduced handgrip strength were further assessed for muscle mass using a Fresenius Body Composition Monitor with multifrequency bioimpedance spectroscopy. ASM was calculated using Lin et al.'s equation[ASM (kg)= -1.838 + 0.395 x total body water(L) + 0.105 x body weight (kg) + 1.231 xmale sex − 0.026 x age (years)] and ASMI was derived by normalizing ASM for height squared( 13 ). Confirmed sarcopenia was diagnosed in patients with both low grip strength and low ASMI. Gait speed was assessed via an 8-meter walk test; speeds < 1.0 m/s confirmed severe sarcopenia( 8 ). Only patients with confirmed or severe sarcopenia were included in the interventional phase. 3. Biochemical Investigations Blood samples were collected for biochemical analysis. Haemoglobin was measured from 2 mL of EDTA-anticoagulated blood using the Vitros 5.1 automated analyser. An additional 3 mL blood in a clot-activated vacutainer was used for measuring serum urea (urease method), creatinine (amino hydrolase method), total protein (Biuret), albumin (bromocresol green), calcium(arsenazo),phosphorus(phosphomolybdate) and 25(OH)D (chemiluminescence). 4. Intervention: Vitamin D Supplementation Patients with confirmed or severe sarcopenia and 25(OH)D levels < 30 ng/mL received oral cholecalciferol 60,000 IU weekly for 12 weeks. Those with levels between 30–60 ng/mL received 60,000 IU every 15 days for 6 weeks. Supplements were administered as sachets dissolved in 200 mL of milk and taken with meals for optimal absorption. Drug adherence was checked by asking patient to bring empty sachet on follow up. 5. Hormonal Profile In sarcopenic patients, a 5 mL fasting pre-dialysis blood sample was drawn. Hormonal assays included total testosterone, LH, FSH, prolactin, insulin, iPTH, cortisol, T3, T4, and TSHmeasured by chemiluminescence. IGF-1 was analysed via ELISA (DRG IGF-1, 600 kit) from 3 mL of serum stored at − 20°C. 6. Quality of Life Assessment The KDQOL-36 (version 1.3) was used to assess quality of life at baseline and 6 months. It included the SF-12 core: PCS (Q1–5, Q8) and MCS (Q6–7, Q9–12), and three CKD-specific subscales—burden of disease (Q13–16), symptoms/problems (Q17–28), and effects on daily life (Q29–36). Each item was scored on a 0–100 scale, with higher scores reflecting better QoL( 14 ). Domain-wise averages were computed for pre- and post-vitamin D supplementation comparisons from baseline to six months. 7. Follow-Up Monitoring Sarcopenia parameters (grip strength, ASMI, gait speed) and biochemical markers (25(OH)D, calcium, phosphorus, iPTH) were reassessed at both 3 and 6 months. Vitamin D dosing was adjusted accordingly: weekly for deficient patients ( 80 ng/ml) or adynamic bone disease(iPTH < 100 pg/ml) was suspected. QoL was reassessed at 6 months using the KDQOL-36. 8.Statistical Methods Data were analysed using IBM SPSS version 20. Normality was assessed using the Kolmogorov–Smirnov test. Categorical variables (e.g., gender, dialysis status, comorbidities, sarcopenia presence) were shown as counts and percentages and tested via Chi-square or Fisher’s exact tests. Continuous variables (e.g., age, BMI, handgrip, ASMI, biochemical markers, QoL scores) were expressed as mean ± SD. Between-group comparisons used independent t-tests or Mann–Whitney U tests, and paired t-tests or Kruskal–Wallis tests for within-group analysis. Repeated measures ANOVA assessed changes over time. Logistic regression was used to identify predictors of baseline sarcopenia and non-responders. Hormonal differences between responders and non-responders were evaluated using t-tests. Correlations between vitamin D and different hormones were assessed using Pearson or Spearman coefficients. A p-value ≤ 0.05 was considered statistically significant. Final analysis was done as per protocol analysis. RESULTS A. Baseline demographics: From 535 screened CKD stage 5 (CKD5) patients, 401 met eligibility and were evaluated for sarcopenia ( Fig. 1 ). Flowchart depicts the screening and classification of 401 CKD patients for sarcopenia based on AWGS 2019 criteria. Muscle strength was assessed via handgrip, muscle mass via ASMI, and severity via gait speed. Sarcopenia was classified as probable, confirmed, or severe. Two patients with vitamin D > 80 ng/mL were excluded. ASMI – appendicular skeletal muscle index, 8MWT- 8-meter walk test. The cohort was predominantly middle-aged with a male majority, and most had low to normal BMI. At baseline, the prevalence of probable, confirmed, and severe sarcopenia was 82.29%, 33.4%, and 25.44%, respectively. CKD5D patients had a slightly higher sarcopenia prevalence than CKD5ND, though not statistically significant ( Table 1 ). Table 1 Prevalence of Sarcopenia Category Total n = 401 n (%) CKD5D (n = 193) n (%) CKD5ND (n = 208) n (%) p value Probable Sarcopenia 330 (82.29%) 162 (83.94%) 168 (80.77%) 0.405 Confirmed Sarcopenia 134 (33.4%) 67(34.71%) 67 (32.21%) 0.595 Severe sarcopenia 102 (25.44%) 53(27.46%) 49(23.56%) 0.370 FOOTNOTES- Sarcopenia was classified according to AWGS 2019 criteria as probable, confirmed, and severe. Values are expressed as n (%). Comparisons between dialysis (CKD5D) and non-dialysis (CKD5ND) groups were made using the chi-square test. A p-value < 0.05 was considered statistically significant. ASMI- appendicular skeletal muscle index, CKD5D- CKD5 patients on dialysis, CKD5ND- not on dialysis. Sarcopenic patients were older, more frequently male, and had lower BMI than non-sarcopenic participants. One-fourth of sarcopenic individuals were overweight or obese, indicating sarcopenic obesity. Comorbidities such as diabetes, hypertension, and CAD were more common in sarcopenic patients. Biochemically, haemoglobin, albumin, and 25(OH)D levels were significantly lower in sarcopenic individuals. MUAC, TTF, and MAMC were similarly reduced. Mean handgrip strength was lowand body composition analysis showed reduced lean tissue mass, fat-free mass, and ASM ( Table 2 ). Table 2 Baseline demographic and clinical profile of in sarcopenic and non-sarcopenic CKD patients Variable Total (n = 401) Mean ± SD, n (%) Sarcopenic (n = 134) Mean ± SD, n (%) Non-Sarcopenic (n = 267) Mean ± SD, n (%) P-value Age (years) 43.95 ± 10.94 44.93 ± 11.00 43.97 ± 10.91 0.264 Male gender 246 (61.35%) 83 (62.4%) 163 (60.8%) 0.862 BMI (Kg/m²) 21.34 ± 4.50 21.03 ± 3.63 21.61 ± 5.15 0.193 Comorbidities Diabetes 173 (43.14%) 66 (49.8%) 107 (40.0%) 0.081 Hypertension 285 (71.07%) 97 (73.2%) 188 (70.0%) 0.678 CAD 23 (5.74%) 17 (12.8%) 6 (2.1%) 0.001* Basic disease DKD 145 (36.16%) 54 (40.30%) 91 (34.08%) 0.226 CGN 111 (27.68%) 32 (23.88%) 79 (29.59%) 0.217 CTID 61 (15.21%) 21 (15.67%) 40 (14.98%) 0.857 ADPKD 44 (10.97%) 17 (12.69%) 27 (10.11%) 0.451 Obstructive nephropathy 40 (9.98%) 10 (7.46%) 30 (11.24%) 0.206 Dialysis parameters Dialysis Access – AVF 171 (42.64%) 60 (45%) 111 (41.6%) 0.007 Dialysis Schedule – Thrice Weekly 212 (52.86%) 77 (40%) 135(65%) 0.004* Biochemical parameters HB 9.16 ± 1.94 8.86 ± 1.87 9.15 ± 2.01 0.154 Creatinine 6.94 ± 3.19 7.09 ± 3.16 6.78 ± 3.22 0.358 Urea 114.59 ± 43.81 113.51 ± 44.97 115.66 ± 42.65 0.646 Total Protein 7.00 ± 0.88 6.90 ± 0.81 7.01 ± 0.94 0.226 Albumin 3.72 ± 0.62 3.74 ± 0.65 3.69 ± 0.58 0.452 SGOT 24.99 ± 01.62 24.31 ± 01.10 25.66 ± 01.13 0.224 SGPT 20.76 ± 11.88 20.62 ± 11.66 20.89 ± 12.10 0.829 Alkaline phosphatase 220.00 ± 13.64 215 ± 11.5 217 ± 13.64 0.124 Calcium 8.10 ± 1.13 8.09 ± 1.02 8.10 ± 1.23 0.931 Phosphorus 4.40 ± 1.39 4.82 ± 1.45 4.68 ± 1.32 0.349 Vitamin D 30.47 ± 2.75 28.30 ± 1.58 32.40 ± 4.70 0.002* iPTH 220.12 ± 35.32 219.23 ± 34.89 221 ± 35.74 0.635 FBS 93.17 ± 2.12 93.90 ± 2.35 92.44 ± 1.89 0.535 HBA1C 5.31 ± 3.36 5.16 ± 3.27 5.45 ± 3.44 0.411 Cholesterol 145.68 ± 7.82 145.69 ± 7.82 145.70 ± 6.87 0.998 Anthropometric Parameters MUAC 25.59 ± 3.58 24.31 ± 3.15 24.84 ± 3.92 0.143 TTF 26.62 ± 3.49 25.52 ± 3.46 25.72 ± 3.52 0.560 MAMC 19.54 ± 3.59 19.39 ± 3.21 19.67 ± 3.91 0.438 Bioimpedance Assay LTM 30.11 ± 01.99 27.74 ± 5.18 32.64 ± 2.54 0.042* LTI 18.15 ± 06.34 17.07 ± 6.99 19.30 ± 2.31 0.237 FFM 15.33 ± 01.04 13.95 ± 0.25 16.49 ± 1.57 0.049* ATM 10.83 ± 0.13 10.31 ± 1.27 11.30 ± 0.99 0.408 FTI 18.34 ± 12.95 17.39 ± 1.03 19.21 ± 2.86 0.230 ASM 13.82 ± 3.14 13.47 ± 3.09 14.17 ± 3.18 0.035* TBW 25.92 ± 5.37 25.39 ± 5.41 26.44 ± 5.32 0.051 OH 1.60 ± 2.59 1.63 ± 2.41 1.56 ± 2.77 0.787 Dry weight 50.74 ± 1.61 51.14 ± 1.16 50.34 ± 1.06 0.451 Sarcopenic parameters Hand grip 18.69 ± 3.80 17.89 ± 3.50 19.89 ± 3.10 0.00* ASMI 7.24 ± 1.53 7.00 ± 1.37 7.48 ± 1.68 .002* FOOTNOTES- Baseline demographic, clinical, biochemical, anthropometric, and bioimpedance parameters were compared between sarcopenic and non-sarcopenic CKD patients. Continuous variables are presented as mean ± standard deviation; categorical variables as n (%). Group comparisons were performed using independent t-test for continuous variables and chi-square test for categorical variables. p < 0.05 was considered statistically significant. BMI- Body mass index, CAD- coronary artery disease, DKD- Diabetic kidney disease, CGN- Chronic glomerulonephritis, CTID- chronic tubulointerstitial nephritis, ADPKD- autosomal dominant polycystic kidney disease, HD- Hemodialysis, AVF – arteriovenous fistula, Hb Haemoglobin, SGOT – serum glutamate oxaloacetic transaminase, SGPT - serum glutamate pyruvic transaminase, ALP- alkaline phosphatase, iPTH- intact parathyroid hormone, FBS- fasting blood glucose, HBA1C – glycated haemoglobin, HDL- high density lipoprotein, LDL- Low density lipoprotein, VLDL- very low-density lipoprotein, TG- triglyceride. MUAC: mid-upper arm circumference; MAMC: mid-arm muscle circumference; TTF: triceps skinfold thickness; LTM: lean tissue mass; LTI: lean tissue index; FFM: fat-free mass; ATM: adipose tissue mass; FTI: fat tissue index; ASM: appendicular skeletal muscle mass; TBW: total body water; OH: overhydration. B. Effect of cholecalciferol supplementation on sarcopenia Cholecalciferol supplementation led to significant functional recovery ( Fig. 2 ). At three months, 13.2% of confirmed sarcopenia patients fully recovered (p = 0.001), and 5.4% improved to probable sarcopenia. At six months, 23.3% fully recovered, and 13.3% moved to the probable category (p = 0.001) ( Table 3 and Figure supplementary SF1). Table 3 Sarcopenia improvement and persistence at 3 month and 6 months after cholecalciferol supplementation Follow-Up Period Total Followed Up Sarcopenic Patients Probable sarcopenia Improved sarcopenia P value At 3-Month Follow-Up 129 105 (81.3%) 7(5.42%) 17(13.17%) 0.001** At 6-Month Follow-Up 120 76(63.3%) 16(13.3%) 28(23.4%) 0.001** FOOTNOTES- Table depicts the change in sarcopenia status at 3-month and 6-month follow-up after cholecalciferol supplementation in CKD stage 5 patients. Values are presented as n (%). Probable sarcopenia was defined as reduced handgrip strength according to AWGS 2019 criteria, improved sarcopenia was defined as meeting higher muscle strength and/or muscle mass thresholds at follow-up compared to baseline. P values represent within-group change over time, calculated using the chi-square test. p < 0.05 indicates statistically significant improvement. At 3rd month follow up, 5 patients loss to follow up and at 6th month 9 patients lost to follow up. Analysis was done as per protocol analysis. Figure shows percentage distribution of sarcopenia classifications at baseline, 3-month, and 6-month follow-up. Blue: sarcopenic patients, Green: probable sarcopenia, Red: improved sarcopenia. Baseline n = 134, 6-month n = 120. P < 0.001. Among severe cases, 30.8% improved their gait speed by three months (p = 0.05), with improvements in 79.8% at six months (p = 0.004). ASMI improved progressively, handgrip strength increased by month 3 and plateaued, and gait speed nearly doubled. BMI, MUAC, MAMC, and TTF all increased significantly over six months (supplementary table S1 and figure SF2). Line graphs represent the mean values of each outcome parameter (ASMI, Handgrip, Gait Speed, BMI, MUAC, MAMC, TTF) at baseline, 3 months, and 6 months. Shaded regions indicate approximate variability around the mean (based on hypothetical standard deviations for visual illustration). Actual p-values are derived from repeated measures ANOVA and post hoc comparisons. Mean vitamin D levels rose from 21.76 ± 13.91 ng/mL at baseline to 38.62 ± 12.94 ng/mL at 3 months (p < 0.0001) and 44.72 ± 13.35 ng/mL at 6 months (p 80 ng/mL), hypercalcemia, hyperphosphatemia, or suppressed iPTH were observed.At 6 months, 83.6% of responder patients were vitamin D sufficient, while 43.5% non-responders remained deficient, suggesting persistent deficiency may contribute to therapeutic failure. Among the responders, it was found that baseline demographics (age, gender, hypertensionand CAD) were similar as non-responders. However, non-responders had significantly higher prevalence of diabetes (66% vs. 34%, p = 0.014) whereas responders had higher baseline handgrip strength (19.2 vs. 15.9 kg, p = 0.008) and ASMI (5.82 vs. 4.90 kg/m², p < 0.001), with greater improvements at follow-up in both handgrip and ASMI (p < 0.001) ( Table 4 ). Table 4 Comparison of Clinical and Hormonal parameters Between Responders and Non-Responders among Sarcopenia Patients Parameter Responder (Mean ± SD) n = 28 Non-Responder (Mean ± SD) n = 92 p-value Age (years) 42.3 ± 8.5 43.1 ± 9.2 0.721 Hypertension, n (%) 27 (97.4%) 81 (88.0%) 0.195 Diabetes, n (%) 18 (64.3%) 75 (81.5%) 0.014 CAD, n (%) 1 (3.6%) 8 (8.7%) 0.367 Gender (Male) n (%) 22 (78.6%) 67 ( 72.8%) 0.807 HANDGRIPV1 19.17 ± 1.89 15.93 ± 1.41 0.008 HANDGRIPV3 26.62 ± 1.70 18.53 ± 1.81 0.00* ASMI1 5.82 ± 0.85 4.90 ± 0.83 0.00* ASMI3 7.05 ± 0.79 5.69 ± 0.73 0.00* TESTOSTERONE 8.56 ± 1.05 9.99 ± 1.05 0.645 LH 13.30 ± 1.84 10.40 ± 1.99 0.104 FSH 13.91 ± 2.75 13.74 ± 1.49 0.952 PROLACTIN 50.30 ± 5.83 66.87 ± 4.82 0.020* INSULIN 10.34 ± 1.38 16.61 ± 2.20 0.209 HOMA-IR 3.01 ± 0.07 4.12 ± 0.70 0.004* IGF1 44.80 ± 3.30 30.60 ± 4.30 0.013* CORTISOL 317.49 ± 18.12 340.34 ± 16.10 0.143 T3 2.71 ± 0.94 1.11 ± 0.94 0.032* T4 0.47 ± 0.90 0.35 ± 0.73 0.434 TSH 6.97 ± 0.84 5.97 ± 0.28 0.419 iPTH 275.93 ± 14.14 190.12 ± 27.28 0.202 Vit.D1 22.40 ± 4.19 17.89 ± 3.07 0.001* Vit.D3 44.31 ± 4.47 26.85 ± 3.07 0.001* FOOTNOTES- Continuous variables are expressed as mean ± SD; categorical variables as n (%). Comparisons between responders and non-responders were made using independent t-test or chi-square test. HANDGRIP1 and ASMI1 refer to baseline handgrip strength and appendicular skeletal muscle index, respectively; HANDGRIP3 and ASMI3 represent values at 6 months. Vit.D1 and Vit.D3 indicate baseline and 6-month vitamin D levels, respectively. p < 0.05 considered statistically significant. p < 0.05* was considered statistically significant. C. Hormonal Abnormalities in Sarcopenic CKD Patients Among sarcopenic patients, IGF-1 deficiency was most common (85%), followed by hyperprolactinemia (68%), subclinical hypothyroidism (56.7%)and insulin resistance (47.5%) ( Table 5 ) . Table 5 Baseline hormonal abnormalities in sarcopenic patients: HORMONE Abnormality Status N (%) Mean ± SD Reference Range Testosterone Deficiency Males − 29 (24.2%) Females − 5 (4.2%) 9.62 ± 1.55 Males: 4.56–28.2 nmol/L Females: 0.2–2.67 nmol/L LH Deficiency Males − 2 (1.7%) Females − 32 (27.1%) 20.03 ± 2.10 Males: 1.8–7.8 m IU/L Females: 1.3–23.4 m IU/L Postmenopausal: 21.5–131 m IU/L FSH Deficiency Males − 41 (34.2%) Females − 5 (4.2%) 13.92 ± 4.78 Males: 1.55–9.74 m IU/L Females: 1.3–23.4 m IU/L Postmenopausal: 21.5–131 m IU/L Prolactin Excess 78 (68.0%) 52.25 ± 4.69 3–18.6 ng/mL Insulin Excess 17 (14.2%) 15.02 ± 2.02 Fasting: 0–24 µIU/mL HOMA-IR High Insulin Resistance 57 (47.5%) 3.84 ± 0.99 Normal: 2.5 IGF-1 Deficiency 103 (85.8%) 34.60 ± 8.30 184–205 ng/mL Cortisol Excess 13 (10.0%) 334.54 ± 18.44 123–626 nmol/L iPTH Excess 51 (42.5%) 219.23 ± 4.89 15–65 pg/mL Thyroid hormone Subclinical Hypothyroid 76 (56.7%) T3 Normal, T4 Normal, High TSH Low T3 Syndrome 14 (10.4%) Low T3, Normal T4, Normal TSH Hypothyroid 20 (14.9%) Low T3, Low T4, High TSH Euthyroid 14 (10.4%) Normal T3, Normal T4, Normal TSH Hyperthyroid 1 (0.7%) High T3, High T4, Low TSH Sick Euthyroid Syndrome 9 (6.7%) Low/Normal T3, Normal T4, Low/Normal TSH FOOTNOTES- Hormonal abnormalities were defined using standard reference ranges. Values are shown as n (%) and mean ± SD. Thyroid dysfunction was classified by T3, T4, and TSH profiles. HOMA-IR > 2.5 indicated insulin resistance.Total Testosterone, Luteinizing Hormone (LH), Follicle-Stimulating Hormone (FSH), Prolactin, Insulin, Insulin-like Growth Factor-1 (IGF-1), Cortisol, Triiodothyronine (T3) (Thyroxine (T4), Thyroid-Stimulating Hormone (TSH), Homeostatic Model Assessment of Insulin Resistance (HOMA-IR). Non-responders showed higher prolactin (66.9 vs. 50.3 ng/mL, p = 0.020), greater insulin resistance (HOMA-IR 4.12 vs. 3.01, p = 0.004), lower T3 (1.11 vs. 2.71, p = 0.032), and lower IGF-1 (44.8 vs. 30.6 ng/mL, p = 0.013). Vitamin D levels were significantly higher in responders, both at baseline (22.4 vs. 17.9 ng/mL, p = 0.001) and after supplementation (44.3 vs. 26.9 ng/mL, p = 0.001). Other hormonal parameters including testosterone, LH, FSH, cortisol, T4, TSH, and iPTH showed no significant differences ( Table 4 ). In vitamin D deficient non-responders, serum 25(OH)D correlated positively with testosterone (r = 0.64, p = 0.032) and IGF-1 (r = 0.76, p = 0.028), and negatively with HOMA-R (r = − 0.61, p = 0.041). These associations highlight a link between low vitamin D, reduced anabolic hormone levels, and insulin resistance. In contrast, among vitamin D sufficient non-responders, IGF-1 showed a paradoxical negative correlation with vitamin D (r = − 0.680, p = 0.046), and no other hormonal markers showed significant associations, suggesting persistent endocrine dysfunction despite vitamin D correction. (Supplementary table S3). D. Associated Risk Factors for sarcopenia For the baseline sarcopenia risk factors, diabetes substantially increased sarcopenia risk and dialysis dependence (OR = 4.0, p = 0.021). Lower MUAC (OR = 1.27, p = 0.006), MAMC (OR = 1.24, p = 0.009), and vitamin D deficiency (OR = 1.045, p = 0.017) also showed significant associations. In multivariate analysis, only diabetes (OR = 9.25, p = 0.004) and vitamin D deficiency (OR = 1.052, p = 0.038) remained independent risk factors (supplementary Table 4a). On logistic regression analysis, several clinical, nutritional, and hormonal factors were associated with non-response to vitamin D supplementation in sarcopenic CKD patients. In the multivariate model, diabetes (OR 2.3, p=0.032) and catheter vascular access (OR 2.98, p=0.041) emerged as independent clinical predictors. Among muscle indices, both reduced handgrip strength (OR 3.95, p=0.003) and lower ASMI (OR 3.6, p=0.005) were strongly associated with poor response. Endocrine and metabolic abnormalities including low testosterone (OR 2.98, p=0.008), high prolactin (OR 2.45, p=0.022), increased HOMA-IR (OR 2.36, p=0.027), and low IGF-1 (OR 2.65, p=0.010) also remained significant predictors.(supplementaryTable 4b) E. Changes in Quality of Life After Supplementation At six months, cholecalciferol supplementation significantly improved KDQOL-36 scores, both physical (PCS) and mental (MCS) components (Table 6 ). No baseline PCS (p = 0.606) or MCS (p = 0.189) differences existed between CKD5D and CKD5ND groups, but both improved post-supplementation in line with physical recovery and biochemical normalization ( Table 6 ). Table 6 Mean improvement in KDQOL − 36 score from baseline to 6 months in sarcopenic after vitamin D supplementation Dialysis Status Measure Timepoint Mean ± SD p-value CKD5D = 67 PCS Baseline 2455.33 ± 602.64 0.05 6 months 2585.58 ± 1019.21 MCS Baseline 3401.39 ± 528.68 0.05 6 months 3523.69 ± 984.89 CKD5ND = 67 PCS Baseline 2534.75 ± 580.54 0.03 6 months 2667.58 ± 929.94 MCS Baseline 3521.44 ± 491.05 0.02 6 months 3657.47 ± 883.46 TOTAL = 134 Physical Baseline 2495.04 ± 590.55 0.00 6 months 2626.58 ± 972.36 Mental Baseline 3461.42 ± 511.63 0.00 6 months 3590.58 ± 934.03 FOOTNOTES- KDQOL-36 scores are reported as mean ± standard deviation (SD). PCS = Physical Component Summary; MCS = Mental Component Summary. Within-group comparisons between baseline and 6-month scores were analyzed using paired t-tests. A p-value < 0.05 was considered statistically significant. DISCUSSION In the absence of specific guidelines by KDIGO or KDOQI on vitamin D supplementation for sarcopenia management, this pragmatic, first-of-its-kind study evaluated sarcopenia prevalence and six months vitamin D supplementation response in CKD5. Study showed, one in three and one in four had sarcopenia and severe sarcopenia respectively, with higher prevalence in dialysis patients. Of them, one-fourth of patients showed significant improvement after vitamin D replacement. Notably, not all patients responded to vitamin D therapy, and non-responders had a higher prevalence of diabetes, elevated hormonal abnormalities, and suboptimal 25(OH)D levels.In persistently vitamin D-deficient non-responders, vitamin D levels positively correlated with IGF-1 and testosterone deficiency and negatively with insulin resistance, hinting at modulation of downstream signalling of these hormones by vitamin D. Relatively higher prevalence of sarcopenia was observed in our study compared to previous studies that documented sarcopenia prevalence ranging from 20–31% in CKD5 patients ( 1 , 15 ).Unlike previous studies, we excluded participants aged more than sixty years due to high primary sarcopenia prevalence in geriatric populations; however, sarcopenia prevalence remained significantly elevated in our younger cohort( 6 ). This reflects both our exclusion criteria and early-onset CKD from inadequately controlled hypertension and diabetes mellitus, likely attributable to regional variations, nutritional deficiencies, delayed nephrology referrals, greater comorbidity burden and methodological differences in our cohort ( 17 ). Male predominance matched local registry data and healthcare-seeking trends, possibly due to faster muscle loss in men driven by testosterone deficiency and heightened catabolism despite greater baseline muscle mass ( 18 ). Although sarcopenia is most common in diabetic kidney disease, followed by hypertension and CAD, it reflects a bidirectional relationship whereby these conditions contribute to muscle wasting through inflammatory mediators (IL-6, TNF-α), vascular dysfunction, and endocrine disturbances( 19 ). A significant number of our study cohort demonstrated lower BMI, reflecting underlying malnutrition. However, BMI proves inadequate for assessing CKD patients as fluid retention and altered body composition due to masking of nutritional status( 20 ). Paradoxically, a subset exhibited sarcopenic obesity, where excess fat infiltration conceals muscle loss. This is consistent with 'hidden sarcopenia' documented in previous CKD studies ( 2 ). Present study has used BIA-based equations for ASMI derivation which is equivalent to gold standard DEXA as validated in dialysis populations (r² = 0.914) and in non-dialysis populations (r = 0.954) ( 13 , 21 ). Only a limited number of clinical studies have evaluated the efficacy of native vitamin D (cholecalciferol) in improving muscle strength and performance in CKD-related sarcopenia with inconsistent results due to variable dosing, duration, and formulation in these studies. Among them two randomized trials done by Hewitt et al. (50000 IU/week for 2 months ; n = 60) and Marckmann et al. (40,000 IU/month for 8 months; n = 52), used cholecalciferol but they failed to demonstrate significant improvements in strength or functional outcomes in dialysis patients despite achieving vitamin D repletion( 4 , 5 ). These results contrast with our study where significant improvement in muscle mass, strength and physical performance was seen. These differences may be due to short term supplementation (2–3 months) which may be insufficient period to detect musculoskeletal improvements, underpowered, utilised fixed non-individualized dosing and absence of sarcopenia-specific inclusion criteria. However, another long term study like ours with high dose cholecalciferol supplementation protocol(50,000 IU weekly adjust levels as per vitamin D levels at 3rd and 6th month for a total of 1 year in haemodialysis patients to see the effect of vitamin D on handgrip strength but it failed to do show any significant difference(geometric mean grip-strength was 27 kg in both groups).The probable explanation was again it was due to less sample size (n = 68) and they supplemented only individuals with baseline vitamin D levels less than 20 ng/ml ( 22 ). However, other long-term intervention studies have shown sarcopenia improvement by supplementing calcitriol in haemodialysis patients and peritoneal dialysis patients as larger thigh‐muscle cross‐sectional area (+ 12%, p < 0.05), greater muscle strength and 67% lower risk of deterioration in muscle mass and function respectively( 23 ). However, they have not used native form of vitamin D and they have not used the established criteria of sarcopenia assessment. Our findings of positive relationship between vitamin D status and muscle strength in CKD populations were also supported by observational studies previously by showing direct association between serum 25(OH)D levels with upper limb handgrip and lower limb quadriceps strength in vitamin D deficit subjects ( 24 , 25 ). In a previous study it was shown that plateau of handgrip strength was seen after achieving threshold value of 30 ng/ml vitamin D which is similar to our study( 26 ). However, in our study in addition to plateaued hand grip strength, muscle mass also improved steadily over six months which might be responsible for sarcopenia improvement. We have also seen vitamin D replacement improves sarcopenia in both vitamin D deficit and sufficient patients without any toxic effects. Our study achieved a level of 44.72 ± 13.35 ng/mL which is similar to Jean et al. who after monthly 100,000 Iu cholecalciferol supplementation for 6 months, serum 25OHD levels increased from 26.8 to 40.8 ± 9.6 ng/ml nmol/L after 6 months, which is far below the toxicity levels (80 ng/ml)( 27 ). Beyond vitamin D deficiency, various endocrine imbalances involving anabolic and catabolic hormones have been implicated in sarcopenia. Our study conducted a comprehensive and analysis of nine different hormones to examine their role in sarcopenic CKD patients especially in vitamin D treatment non responsive sarcopenic patients.Aligning with our study of higher prevalence of hypogonadism in both in haemodialysis and non-dialysis males subjects, however a Turkish study has shown a higher prevalence in haemodialysis subjects only ( 28 ). In our cohort of sarcopenic patients, we have observed lower mean testosterone and gonadotropins levels both in males and females. Our findings align previous trials who have shown a negative correlation between endogenous testosterone levels and gonadotropin levels with worsening CKD stages( 29 ). Gonadotropin deficiencies were observed in a sex-specific pattern. LH and FSH suppression were more prominent in females mirroring previous reports of uremic-induced hypothalamic–pituitary axis disruption more in females ( 30 ) . Similar to the standard thyroid abnormalities in CKD patients, we also found subclinical hypothyroidism (50%) followed by low T3 syndrome (10%) in our patients. Abhilash et al., also found the similar thyroid abnormality aligning to ours ( 31 ). Hyperprolactinemia was identified in one in seventh patient of our cohort, consistent with previous data reporting prolactin excess in 60% -70% of patients on maintenance dialysis attributable to both reduced renal clearance and increased pituitary secretion, with adverse effects on gonadal function and subsequently muscle health ( 32 ). IGF-1 deficiency emerged as the most prevalent hormonal abnormality in our cohort, affecting 85.8% of patients, consistent with an Indonesian study of elderly dialysis patients with sarcopenia, where IGF-1 suppression was similarly prominent and mean IGF-1 level in our population (34.60 ± 68.30 ng/mL) closely matched that of their sarcopenic subgroup (33.43 ng/mL)( 33 ). However, our cohort was younger (< 60 years), and the prevalence of sarcopenia among dialysis patients was lower (34.7% vs. 82.5%), likely reflecting both age-related differences in IGF-1 levels and the progressive decline in IGF-1 following dialysis initiationas demonstrated in earlier studies reporting up to a 33% reduction in IGF-1 levels after the onset of dialysis. We have observed that almost half of the sarcopenic patients had high insulin resistance with HOMA-IR of 3.84 against cutoff value of > 2.5, based on a study done by Li et al ( 34 ).This is aligning with a prior studyby Srinowati et al. who reported 77.5% prevalence of insulin resistance with elevated HOMA-IR of 2.29 against to their lower cutoff of > 1.56among elderly haemodialysis patients( 35 ). Despite achieving sufficient vitamin D levels after six months of supplementation, nearly half of the non-responders showed no improvement, likely due to persistent hormonal abnormalities. IGF-1 deficiency, testosterone deficiency, and insulin resistance were significantly associated with poor treatment response. Among vitamin D–deficient non-responders, lower vitamin D levels correlated positively with IGF-1 and testosterone deficiency, and negatively with insulin resistance, suggesting a key hormonal influence on treatment failure. While the direct link between vitamin D, testosterone, and sarcopenia in CKD is not fully established, it is plausible that vitamin D deficiency may negatively impact testosterone production or its effects on muscle, exacerbating sarcopenia. Some research suggests that testosterone may enhance the effects of vitamin D on muscle strength as shown in recent meta-analysis of 15 non- CKD studies. They confirmed that vitamin D supplementation significantly increases total testosterone levels, particularly with durations exceeding 12 weeks and dosages above 4000 IU/day( 36 ). The proposed mechanism suggested involves vitamin D receptors and metabolizing enzymes expressed in Leydig cells of the testis, where vitamin D can directly influence testosterone production in human testicular cell cultures as shown in a castrated mice model( 35 ). Our study reveals a critical biphasic vitamin D–IGF-1 relationship in sarcopenic patients, with a positive correlation in vitamin D–deficient non-responders and negative correlation in vitamin D–sufficient non-responders. This finding aligns with Li & Yu’s NHANES III analysis demonstrating a positive correlation below 75 nmol/L (β = 0.16, p = 0.0103) but negative correlation above this threshold (β = −0.53, p = 0.0057) ( 37 )Another showed IGF-1 plateauing at 75–85 nmol/L with reduced metabolic efficacy thereafter ( 38 ). Mendelian randomization confirms a bidirectional causal relationship, with IGF-1 stimulating 1-α-hydroxylase and vitamin D receptors enhancing IGF-1 concentrations ( 39 ). Probable mechanisms for the deficient non-responder positive correlation include less compensatory IGF-1 levels restoring the disrupted axis, downregulated 1-α-hydroxylase activity, and reduced IGF-1 receptor sensitivity in vitamin D–starved muscle as hypothesised by Vicinanza et al( 40 ). Conversely, the sufficient non-responder negative correlation reflects vitamin D–induced IGF-1 receptor desensitization through VDR overexpression, altered IGF binding protein ratios reducing bioavailable IGF-1, established myostatin elevation in advanced sarcopenia and dose–duration effects where supplementation > 1,000 IU/day for > 12 weeks produces negative IGF-1 associations ( 41 ). However, Trummer et al.’s RCT showed no correlation between baseline IGF-1 and 25(OH)D (r = − 0.008, p = 0.91) but significant correlation with active 1,25(OH)₂D (r = 0.21, p = 0.005) but notably they excluded patients with egfr < 15 ml/min( 42 ). Our findings support shifting from routine supplementation to precision therapy, targeting 50–75 nmol/L vitamin D, with IGF-1 as a biomarker and individualized strategies. An inverse association between 25(OH)D and insulin resistance mirroring our finding where insulin resistance (QUICKI index) correlated negatively with serum 25(OH)D ( 43 ). However, this study was done in early CKD stage unlike our advanced satge. In large NHANES III CKD subanalysis it was reported that participants with both reduced eGFR and lower 25(OH)D independently predicted higher HOMA-IR ( 44 ). At baseline, KDQOL-36 scores revealed no significant differences in PCS or MCS scores between sarcopenic CKD5D and CKD5ND patients, indicating comparable health-related quality of life (HRQoL). This finding is consistent with Manavalan et al., who identified kidney disease component summary score (KDCS) showed a significant decline (P = 0.01) from CKD 3 to CKD 5D whereas MCS and PCS showed a nonsignificant decrease( 45 ). Following six months of vitamin D supplementation, both PCS and MCS improved significantly from baseline in our cohort which contrast prior evidence linking vitamin D therapy to improved QoL. like Hewitt et al. and Singer et al. who found no QoL benefit despite correcting severe deficiency over 12 months ( 5 , 22 ). These discrepancies may reflect heterogeneity in dosing regimens, baseline deficiency severity, and study durations. The study novelties include long term vitamin D supplementation, first to comprehensively evaluate nine-hormonal axis,finding causes of vitamin D non-responsiveness, appropriately supplementing in baseline vitamin D sufficient individuals without toxicity and used bedside applicable bioimpedance derived equation for sarcopenia diagnosis. Key limitations include lack of randomisation for vitamin D supplementation, absent nutritional and exercise history, sample size for evaluating the effect of hormones on sarcopenia was limited except vitamin D. Conclusion Sarcopenia and vitamin D deficiency are highly prevalent in CKD patients. Longer duration, tailored cholecalciferol therapy improves sarcopenic parameters along with mental and physical components of QoL. Persistent hormonal imbalances like IGF-1 deficiency, testosterone deficiency and insulin resistance may limit full therapeutic efficacy of vitamin D among non-responders. These findings highlightthe need for future multidisciplinary approach integrating vitamin D with hormonal association, nutritional support, and physical rehabilitation to effectively counteract sarcopenia in this vulnerable population. Abbreviations • CKD chronic kidney disease • BMI Body Mass Index • DEXA Dual–Energy X–ray Absorptiometry • CT Computed Tomography • MRI Magnetic Resonance Imaging • BIA Bioelectrical Impedance Analysis • IGF 1 –Insulin–like Growth Factor 1 • PTH Parathyroid Hormone • VDR Vitamin D Receptor • AWGS Asian Working Group for Sarcopenia • ASMI Appendicular Skeletal Muscle Index • MUAC Mid–Upper Arm Circumference • TFF Triceps Fat Fold • MAMC Mid–Arm Muscle Circumference • ESRD End–Stage Renal Disease • ANOVA Analysis of Variance • ASM Appendicular Skeletal Muscle Mass • EDTA Ethylenediaminetetraacetic Acid • 25(OH)D 25–hydroxyvitamin D • LH Luteinizing Hormone • FSH Follicle–Stimulating Hormone • iPTH Intact Parathyroid Hormone • T3 Triiodothyronine • T4 Thyroxine • TSH Thyroid–Stimulating Hormone • ELISA Enzyme–Linked Immunosorbent Assay • KDQOL 36 –Kidney Disease Quality of Life–36 Questionnaire • SF 12 –Short Form–12 Questionnaire • PCS Physical Component Summary • MCS Mental Component Summary • IBM SPSS International Business Machines Statistical Package for the Social Sciences • CAD coronary artery disease • AV fistula Arteriovenous Fistula • HOMA R / HOMA – IR –Homeostasis Model Assessment of Insulin Resistance • KDIGO Kidney Disease Improving Global Outcomes • KDOQI Kidney Disease Outcomes Quality Initiative • IL 6 –Interleukin–6 • TNF α –Tumor Necrosis Factor–alpha • r² Coefficient of Determination • RCT Randomized Controlled Trial • eGFR Estimated Glomerular Filtration Rate • NHANES National Health and Nutrition Examination Survey • HRQoL Health–Related Quality of Life • KDCS Kidney Disease Component Summary Declarations Ethics approval and consent to participate: Ethical Committee clearance from institutional committee of ABVIMs, Dr. R.M.L. Hospital vide number F.No TP(DM/Mch) 31/2023/IEC/ABVIMS/1406 dated 3 rd August 2023. This study was conducted in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards. Trial Registery- Clinical Trial Registery (India) CTRI – CTRI/2025/08/092512 – DATED 6 TH AUGUST 2025( retrospectively enrolled) Written informed consent was acquired from the participants prior to their inclusion in the study. All methods were carried out in accordance with relevant guidelines and protocols. Consent for publication: Not applicable Availability of data and materials: yes data will be shared when asked Competing interests: we have no competing interest. Funding: not applicable Authors' contributions: Author I: Dr. Disha Arora: Conceptualization , Formal analysis, Writing - Original Draft. Author II:Dr. Lalit Pursnani: Methodology, Validation, Formal analysis, Data Curation. Author III: Dr. Himansu Sekhar Mahapatra: : I nvestigation, Resources, Writing - Review& Editing. (CORRESPONDING AUTHOR) Author IV : Dr. MuthuKumar Balakrishnan: Supervision, Project administration, Critical revision of the manuscript. Author V: Dr. Renju Binoy: Patient recruitment, Clinical data acquisition, Investigation. Author VI: Dr. Lokesh Kumar Sharma: Biochemical analysis, Data interpretation, Validation. Other authors: Dr. Hari, Dr. Varuna, and Dr. Vipin: Patient management, Data collection, Resources . Dr. Lakshman and Dr. Chandra Krishnan: Statistical analysis. Acknowledgements: Professor Venkateshan Sekhar, management consultant for helping in statistical analysis. Mr. Sourabh and Miss Deepshikha for helping in Quality-of-life survey and drug adherence follow up. References Duarte MP, Almeida LS, Neri SGR, Oliveira JS, Wilkinson TJ, Ribeiro HS, et al. 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Assessment of health-related quality of life and its determinants in patients with chronic kidney disease. Indian J Nephrol. 2017;27(1):37. Additional Declarations No competing interests reported. Supplementary Files SupplementaryInfo.docx Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 17 Oct, 2025 Reviewers agreed at journal 08 Oct, 2025 Reviewers invited by journal 06 Oct, 2025 Editor invited by journal 09 Sep, 2025 Editor assigned by journal 25 Aug, 2025 Submission checks completed at journal 25 Aug, 2025 First submitted to journal 22 Aug, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7434137","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":530774746,"identity":"4bcbb589-2e8c-4543-89a5-32296e3e4c6a","order_by":0,"name":"DISHA ARORA","email":"","orcid":"","institution":"Dr. Ram Manohar Lohia Hospital","correspondingAuthor":false,"prefix":"","firstName":"DISHA","middleName":"","lastName":"ARORA","suffix":""},{"id":530774748,"identity":"c3f06c4c-245c-4d92-a222-b9a4b47200c1","order_by":1,"name":"LALIT PURSNANI","email":"","orcid":"","institution":"Dr. Ram Manohar Lohia 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15:48:04","extension":"html","order_by":14,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":225117,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-7434137/v1/8a49c249d071a804ff781c37.html"},{"id":93795308,"identity":"d9f54cb4-0004-4bf0-961a-bb8541a455ed","added_by":"auto","created_at":"2025-10-17 15:48:03","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":79849,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eshowing prevalence of sarcopenia\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFlowchart depicts the screening and classification of 401 CKD patients for sarcopenia based on AWGS 2019 criteria. Muscle strength was assessed via handgrip, muscle mass via ASMI, and severity via gait speed. Sarcopenia was classified as probable, confirmed, or severe. Two patients with vitamin D \u0026gt;80 ng/mL were excluded. ASMI – appendicular skeletal muscle index, 8MWT- 8-meter walk test.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-7434137/v1/fb15d67674ff08707e0b4f0f.png"},{"id":93797246,"identity":"2337e8eb-ceaa-46eb-852b-e0985ef1a144","added_by":"auto","created_at":"2025-10-17 15:56:03","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":130187,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eshowing study algorithm for vitamin D supplementation in Sarcopenic CKD5 patients: \u003c/strong\u003eFlowchart shows follow-up of 134 sarcopenic CKD patients over 6 months after cholecalciferol supplementation. Patients were classified as vitamin D deficient (\u0026lt;30 ng/mL) or sufficient (≥30 ng/mL) and treated accordingly. Sarcopenia status was reassessed at 3 and 6 months using handgrip and ASMI per AWGS 2019 criteria. Outcomes were categorized as improved sarcopenia, probable sarcopenia, or persistent sarcopenia. Dropouts and vitamin D status at each stage are indicated.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-7434137/v1/b3ceaf3e63ddb7e86786b7d5.png"},{"id":93798598,"identity":"4a1261dc-4618-4212-bf06-83abf06021ea","added_by":"auto","created_at":"2025-10-17 16:12:04","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2185019,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7434137/v1/6165bd84-13a4-4ef2-9137-a5a61ccda9a7.pdf"},{"id":93795316,"identity":"84a55985-4cab-4acd-9263-5fdbf6656529","added_by":"auto","created_at":"2025-10-17 15:48:04","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":266056,"visible":true,"origin":"","legend":"","description":"","filename":"SupplementaryInfo.docx","url":"https://assets-eu.researchsquare.com/files/rs-7434137/v1/4f60cc2993f22e40ef06df39.docx"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003eRelationship of Different Hormone levelsand Effect of six-month Cholecalciferol Supplementationin Sarcopenic End-Stage Kidney Disease: A prospective interventional study\u003c/p\u003e","fulltext":[{"header":"Background","content":"\u003cp\u003eSarcopenia, marked by the progressive loss of muscle mass, strength, and function, is a frequent but underrecognized complication of chronic kidney disease CKD. Although, exact prevalence in different stages of CKD is understudied, existing literature showed it is prevalent as 5.9\u0026ndash;28.7% of patients with stage 5 CKD not on dialysis and nearly 25.9\u0026ndash;34.6%of those on dialysis(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Beyond its association with frailty and higher mortality, sarcopenia significantly impairs quality of life (QoL) by limiting physical performance and increasing hospitalization risk. Despite these consequences, routine screening remains limited, particularly in resource-constrained settings where body mass index (BMI) and fluid overload obscure muscle loss. Conventional tools such as DEXA scan are affected by fluid status, CT and MRI are costly, while bioelectrical impedance analysis (BIA), though feasible, lacks CKD-specific validation, underscoring the need for simple bedside tools for early diagnosis (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eUnlike age-related sarcopenia, uremic sarcopenia develops early due to inflammation, uremic toxins, protein-energy wasting, and endocrine dysfunction. An imbalance between anabolic hormones (IGF-1, testosterone, oestrogen, thyroid) and catabolic mediators (cortisol, PTH) drives muscle degradation. Further, vitamin D deficiency, nearly universal in CKD,worsens muscle health by impairing VDR-mediated pathways controlling protein synthesis, mitochondrial activity, and myogenesis(\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Clinical trials of cholecalciferol for sarcopenia in CKD showed inconsistent outcomes, largely due to variability in CKD stage, dosing, formulations, baseline vitamin D status, and assessment methods(\u003cspan additionalcitationids=\"CR5\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eVitamin D also modulates multiple hormonal axes, enhancing IGF-1, stimulating testosterone, improving insulin sensitivity, suppressing cortisol, reducing PTH, and stabilizing thyroid and prolactin levels, thereby preserving muscle integrity (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Despite growing evidence of vitamin D\u0026rsquo;s influence on these pathways, its role in reversing sarcopenia remains poorly understood. Persistent anabolic resistance may blunt its therapeutic effects, highlighting the need for studies that integrate both functional and hormonal abnormalities.\u003c/p\u003e\u003cp\u003eTo address these gaps, our study examines the long-term effects of individualized cholecalciferol supplementation on muscle mass, strength, and QoL in sarcopenic CKD patients. By integrating detailed hormonal profiling, we aim to clarify how vitamin D interacts with endocrine pathways and identify predictors of treatment response.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003e\u003cstrong\u003eStudy Design and Duration\u003c/strong\u003e\u003cp\u003eThis was a prospective, interventional study conducted over a six-month period in the Department of Nephrology at a tertiary care centre.\u003c/p\u003e\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eInclusion and Exclusion Criteria\u003c/strong\u003e\u003cp\u003e Patients aged 18 to 60 years with CKD stage 5, attending either nephrology outpatient services or undergoing maintenance haemodialysis in the dialysis unit, were enrolled after providing written informed consent. Patients were excluded if they were bedridden or unable to perform physical function assessments, had any active malignancy, HIV, tuberculosis, chronic liver disease, or were pregnant. Additional exclusions included the presence of implanted cardiac devices that contraindicated the use of bioimpedance analysis, any known endocrine abnormality apart from diabetes mellitus, and the intake of vitamin D supplements, calcium-based phosphate binders, or corticosteroids within three months prior to enrolment.\u003c/p\u003e\u003c/p\u003e\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003eDefinitions\u003c/h2\u003e\u003cp\u003e\u003cul\u003e\u003cli\u003e\u003cp\u003e\u003cb\u003eSarcopenia\u003c/b\u003e was defined using the AWGS 2019 consensus. Probable sarcopenia was diagnosed when grip strength was low (\u0026lt;\u0026thinsp;28 kg in men and \u0026lt;\u0026thinsp;18 kg in women). Confirmed sarcopenia required low grip strength along with low appendicular skeletal muscle index (ASMI\u0026thinsp;\u0026lt;\u0026thinsp;7.0 kg/m\u0026sup2; in men, \u0026lt;\u0026thinsp;5.7 kg/m\u0026sup2; in women). Severe sarcopenia further included low gait speed (\u0026lt;\u0026thinsp;1.0 m/s)(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e).\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003e\u003cb\u003eBody Mass Index (BMI)\u003c/b\u003e was categorized based on Asian standards: \u0026lt;18.5 as underweight, 18.5\u0026ndash;22.9 as normal, 23\u0026ndash;24.9 as overweight, 25\u0026ndash;29.9 as obese class I, and \u0026ge;\u0026thinsp;30 kg/m\u0026sup2; as obese class II(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e).\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003e\u003cb\u003eMid-upper arm circumference (MUAC)\u003c/b\u003e was considered low at \u0026le;\u0026thinsp;28.6 cm in men and \u0026le;\u0026thinsp;27.5 cm in women.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003e\u003cb\u003eTriceps fat fold (TFF)\u003c/b\u003e define fat depletion was taken as \u0026lt;\u0026thinsp;10 mm in men and \u0026lt;\u0026thinsp;13 mm in women.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003e\u003cb\u003eMid-arm muscle circumference (MAMC)\u003c/b\u003e was calculated as MUAC-3.1415 x TFF. Severe malnutrition was considered as MAMC\u0026thinsp;\u0026lt;\u0026thinsp;19 cmin men and \u0026lt;\u0026thinsp;16 cm in women.\u003c/p\u003e\u003c/li\u003e\u003c/ul\u003e\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003eSample Size Calculation\u003c/h3\u003e\n\u003cp\u003eSample size was based on the study by Wang et al., which examined the effects of oral cholecalciferol on sarcopenia in ESRD patients(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). Using G*Power software with repeated measures ANOVA at three time points (baseline, 3 months, and 6 months), assuming an effect size of 0.5, significance level (α) of 0.05, and power of 90%, a minimum of 96 participants were required. With a 20% attrition adjustment, the target sample size was 116. Based on sarcopenia prevalence of 25\u0026ndash;40% among CKD5 patients, approximately 300\u0026ndash;480 patients were planned for screening. Further, for hormonal assessment, sample size was calculated for each of the nine hormones we used in the study and sample size ranged from minimum of 171 to maximum of 346 (\u003cspan additionalcitationids=\"CR11\" citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e), however study remains underpowered for hormone analysis.\u003c/p\u003e\u003cp\u003e\u003cb\u003eData Collection\u003c/b\u003e\u003c/p\u003e\u003cp\u003e\u003cb\u003e1. Demographic and Clinical Examination\u003c/b\u003e\u003c/p\u003e\u003cp\u003eBaseline data including age, sex, and known comorbidities (e.g., diabetes, hypertension, cardiovascular disease) were recorded. Aetiology of CKD was determined from clinical history or previous renal biopsy. For dialysis patients- access (AV fistula or catheter), frequency (2\u0026ndash;3 sessions weekly), and dialysis vintage were documented. Anthropometric measurements included height, weight, BMI, MUAC, TFF, and MAMC.\u003c/p\u003e\u003cp\u003e\u003cb\u003e2. Sarcopenia Diagnosis\u003c/b\u003e\u003c/p\u003e\u003cp\u003eHandgrip strength was measured using a handheld dynamometer on the dominant or non-fistula arm, in a seated position with the elbow flexed at 90\u0026deg;. The average of three readings, spaced one minute apart was used. Patients with reduced handgrip strength were further assessed for muscle mass using a Fresenius Body Composition Monitor with multifrequency bioimpedance spectroscopy. ASM was calculated using Lin et al.'s equation[ASM (kg)= -1.838\u0026thinsp;+\u0026thinsp;0.395 x total body water(L)\u0026thinsp;+\u0026thinsp;0.105 x body weight (kg)\u0026thinsp;+\u0026thinsp;1.231 xmale sex \u0026minus;\u0026thinsp;0.026 x age (years)] and ASMI was derived by normalizing ASM for height squared(\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Confirmed sarcopenia was diagnosed in patients with both low grip strength and low ASMI. Gait speed was assessed via an 8-meter walk test; speeds\u0026thinsp;\u0026lt;\u0026thinsp;1.0 m/s confirmed severe sarcopenia(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Only patients with confirmed or severe sarcopenia were included in the interventional phase.\u003c/p\u003e\u003cp\u003e\u003cb\u003e3. Biochemical Investigations\u003c/b\u003e\u003c/p\u003e\u003cp\u003eBlood samples were collected for biochemical analysis. Haemoglobin was measured from 2 mL of EDTA-anticoagulated blood using the Vitros 5.1 automated analyser. An additional 3 mL blood in a clot-activated vacutainer was used for measuring serum urea (urease method), creatinine (amino hydrolase method), total protein (Biuret), albumin (bromocresol green), calcium(arsenazo),phosphorus(phosphomolybdate) and 25(OH)D (chemiluminescence).\u003c/p\u003e\u003cp\u003e\u003cb\u003e4. Intervention: Vitamin D Supplementation\u003c/b\u003e\u003c/p\u003e\u003cp\u003ePatients with confirmed or severe sarcopenia and 25(OH)D levels\u0026thinsp;\u0026lt;\u0026thinsp;30 ng/mL received oral cholecalciferol 60,000 IU weekly for 12 weeks. Those with levels between 30\u0026ndash;60 ng/mL received 60,000 IU every 15 days for 6 weeks. Supplements were administered as sachets dissolved in 200 mL of milk and taken with meals for optimal absorption. Drug adherence was checked by asking patient to bring empty sachet on follow up.\u003c/p\u003e\u003cp\u003e\u003cb\u003e5. Hormonal Profile\u003c/b\u003e\u003c/p\u003e\u003cp\u003eIn sarcopenic patients, a 5 mL fasting pre-dialysis blood sample was drawn. Hormonal assays included total testosterone, LH, FSH, prolactin, insulin, iPTH, cortisol, T3, T4, and TSHmeasured by chemiluminescence. IGF-1 was analysed via ELISA (DRG IGF-1, 600 kit) from 3 mL of serum stored at \u0026minus;\u0026thinsp;20\u0026deg;C.\u003c/p\u003e\u003cp\u003e\u003cb\u003e6. Quality of Life Assessment\u003c/b\u003e\u003c/p\u003e\u003cp\u003eThe KDQOL-36 (version 1.3) was used to assess quality of life at baseline and 6 months. It included the SF-12 core: PCS (Q1\u0026ndash;5, Q8) and MCS (Q6\u0026ndash;7, Q9\u0026ndash;12), and three CKD-specific subscales\u0026mdash;burden of disease (Q13\u0026ndash;16), symptoms/problems (Q17\u0026ndash;28), and effects on daily life (Q29\u0026ndash;36). Each item was scored on a 0\u0026ndash;100 scale, with higher scores reflecting better QoL(\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Domain-wise averages were computed for pre- and post-vitamin D supplementation comparisons from baseline to six months.\u003c/p\u003e\u003cp\u003e\u003cb\u003e7. Follow-Up Monitoring\u003c/b\u003e\u003c/p\u003e\u003cp\u003eSarcopenia parameters (grip strength, ASMI, gait speed) and biochemical markers (25(OH)D, calcium, phosphorus, iPTH) were reassessed at both 3 and 6 months. Vitamin D dosing was adjusted accordingly: weekly for deficient patients (\u0026lt;\u0026thinsp;30 ng/mL), every 15 days for sufficient levels (30\u0026ndash;80 ng/mL) at 3rd month, and discontinued if toxicity(vitamin D\u0026thinsp;\u0026gt;\u0026thinsp;80 ng/ml) or adynamic bone disease(iPTH\u0026thinsp;\u0026lt;\u0026thinsp;100 pg/ml) was suspected. QoL was reassessed at 6 months using the KDQOL-36.\u003c/p\u003e\u003cp\u003e\u003cb\u003e8.Statistical Methods\u003c/b\u003e\u003c/p\u003e\u003cp\u003eData were analysed using IBM SPSS version 20. Normality was assessed using the Kolmogorov\u0026ndash;Smirnov test. Categorical variables (e.g., gender, dialysis status, comorbidities, sarcopenia presence) were shown as counts and percentages and tested via Chi-square or Fisher\u0026rsquo;s exact tests. Continuous variables (e.g., age, BMI, handgrip, ASMI, biochemical markers, QoL scores) were expressed as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD. Between-group comparisons used independent t-tests or Mann\u0026ndash;Whitney U tests, and paired t-tests or Kruskal\u0026ndash;Wallis tests for within-group analysis. Repeated measures ANOVA assessed changes over time. Logistic regression was used to identify predictors of baseline sarcopenia and non-responders. Hormonal differences between responders and non-responders were evaluated using t-tests. Correlations between vitamin D and different hormones were assessed using Pearson or Spearman coefficients. A p-value\u0026thinsp;\u0026le;\u0026thinsp;0.05 was considered statistically significant. Final analysis was done as per protocol analysis.\u003c/p\u003e"},{"header":"RESULTS","content":"\u003cdiv id=\"Sec6\" class=\"Section2\"\u003e\n \u003ch2\u003eA. Baseline demographics:\u003c/h2\u003e\n \u003cp\u003eFrom 535 screened CKD stage 5 (CKD5) patients, 401 met eligibility and were evaluated for sarcopenia \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003eFlowchart depicts the screening and classification of 401 CKD patients for sarcopenia based on AWGS 2019 criteria. Muscle strength was assessed via handgrip, muscle mass via ASMI, and severity via gait speed. Sarcopenia was classified as probable, confirmed, or severe. Two patients with vitamin D\u0026thinsp;\u0026gt;\u0026thinsp;80 ng/mL were excluded. ASMI \u0026ndash; appendicular skeletal muscle index, 8MWT- 8-meter walk test.\u003c/p\u003e\n \u003cp\u003eThe cohort was predominantly middle-aged with a male majority, and most had low to normal BMI. At baseline, the prevalence of probable, confirmed, and severe sarcopenia was 82.29%, 33.4%, and 25.44%, respectively. CKD5D patients had a slightly higher sarcopenia prevalence than CKD5ND, though not statistically significant \u003cstrong\u003e(\u003c/strong\u003eTable\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab1\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003ePrevalence of Sarcopenia\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCategory\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003cp\u003en\u0026thinsp;=\u0026thinsp;401\u003c/p\u003e\n \u003cp\u003en (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCKD5D\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;193)\u003c/p\u003e\n \u003cp\u003en (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCKD5ND\u003c/p\u003e\n \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;208)\u003c/p\u003e\n \u003cp\u003en (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eProbable Sarcopenia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e330 (82.29%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e162 (83.94%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e168 (80.77%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.405\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eConfirmed Sarcopenia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e134 (33.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e67(34.71%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e67 (32.21%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.595\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSevere sarcopenia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e102 (25.44%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e53(27.46%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e49(23.56%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.370\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003eFOOTNOTES- Sarcopenia was classified according to AWGS 2019 criteria as probable, confirmed, and severe. Values are expressed as n (%). Comparisons between dialysis (CKD5D) and non-dialysis (CKD5ND) groups were made using the chi-square test. A p-value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant. ASMI- appendicular skeletal muscle index, CKD5D- CKD5 patients on dialysis, CKD5ND- not on dialysis.\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003cp\u003eSarcopenic patients were older, more frequently male, and had lower BMI than non-sarcopenic participants. One-fourth of sarcopenic individuals were overweight or obese, indicating sarcopenic obesity. Comorbidities such as diabetes, hypertension, and CAD were more common in sarcopenic patients. Biochemically, haemoglobin, albumin, and 25(OH)D levels were significantly lower in sarcopenic individuals. MUAC, TTF, and MAMC were similarly reduced. Mean handgrip strength was lowand body composition analysis showed reduced lean tissue mass, fat-free mass, and ASM \u003cstrong\u003e(\u003c/strong\u003eTable\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab2\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eBaseline demographic and clinical profile of in sarcopenic and non-sarcopenic CKD patients\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eVariable\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTotal (n\u0026thinsp;=\u0026thinsp;401) Mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD, n (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eSarcopenic (n\u0026thinsp;=\u0026thinsp;134) Mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD, n (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eNon-Sarcopenic (n\u0026thinsp;=\u0026thinsp;267) Mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD, n (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e43.95\u0026thinsp;\u0026plusmn;\u0026thinsp;10.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e44.93\u0026thinsp;\u0026plusmn;\u0026thinsp;11.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e43.97\u0026thinsp;\u0026plusmn;\u0026thinsp;10.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.264\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMale gender\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e246 (61.35%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e83 (62.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e163 (60.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.862\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBMI (Kg/m\u0026sup2;)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21.34\u0026thinsp;\u0026plusmn;\u0026thinsp;4.50\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21.03\u0026thinsp;\u0026plusmn;\u0026thinsp;3.63\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21.61\u0026thinsp;\u0026plusmn;\u0026thinsp;5.15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.193\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eComorbidities\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDiabetes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e173 (43.14%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e66 (49.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e107 (40.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.081\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypertension\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e285 (71.07%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e97 (73.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e188 (70.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.678\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCAD\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e23 (5.74%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17 (12.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 (2.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.001*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eBasic disease\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDKD\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e145 (36.16%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e54 (40.30%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e91 (34.08%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.226\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCGN\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e111 (27.68%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e32 (23.88%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e79 (29.59%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.217\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCTID\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e61 (15.21%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21 (15.67%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e40 (14.98%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.857\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eADPKD\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e44 (10.97%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17 (12.69%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e27 (10.11%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.451\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eObstructive nephropathy\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e40 (9.98%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10 (7.46%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e30 (11.24%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.206\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eDialysis parameters\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDialysis Access \u0026ndash; AVF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e171 (42.64%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e60 (45%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e111 (41.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.007\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDialysis Schedule \u0026ndash; Thrice Weekly\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e212 (52.86%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e77 (40%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e135(65%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.004*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eBiochemical parameters\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHB\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9.16\u0026thinsp;\u0026plusmn;\u0026thinsp;1.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8.86\u0026thinsp;\u0026plusmn;\u0026thinsp;1.87\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9.15\u0026thinsp;\u0026plusmn;\u0026thinsp;2.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.154\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCreatinine\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6.94\u0026thinsp;\u0026plusmn;\u0026thinsp;3.19\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.09\u0026thinsp;\u0026plusmn;\u0026thinsp;3.16\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6.78\u0026thinsp;\u0026plusmn;\u0026thinsp;3.22\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.358\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eUrea\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e114.59\u0026thinsp;\u0026plusmn;\u0026thinsp;43.81\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e113.51\u0026thinsp;\u0026plusmn;\u0026thinsp;44.97\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e115.66\u0026thinsp;\u0026plusmn;\u0026thinsp;42.65\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.646\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTotal Protein\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.00\u0026thinsp;\u0026plusmn;\u0026thinsp;0.88\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6.90\u0026thinsp;\u0026plusmn;\u0026thinsp;0.81\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.01\u0026thinsp;\u0026plusmn;\u0026thinsp;0.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.226\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAlbumin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.72\u0026thinsp;\u0026plusmn;\u0026thinsp;0.62\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.74\u0026thinsp;\u0026plusmn;\u0026thinsp;0.65\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.69\u0026thinsp;\u0026plusmn;\u0026thinsp;0.58\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.452\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSGOT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24.99\u0026thinsp;\u0026plusmn;\u0026thinsp;01.62\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24.31\u0026thinsp;\u0026plusmn;\u0026thinsp;01.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.66\u0026thinsp;\u0026plusmn;\u0026thinsp;01.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.224\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSGPT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20.76\u0026thinsp;\u0026plusmn;\u0026thinsp;11.88\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20.62\u0026thinsp;\u0026plusmn;\u0026thinsp;11.66\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20.89\u0026thinsp;\u0026plusmn;\u0026thinsp;12.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.829\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAlkaline phosphatase\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e220.00\u0026thinsp;\u0026plusmn;\u0026thinsp;13.64\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e215\u0026thinsp;\u0026plusmn;\u0026thinsp;11.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e217\u0026thinsp;\u0026plusmn;\u0026thinsp;13.64\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.124\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCalcium\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8.10\u0026thinsp;\u0026plusmn;\u0026thinsp;1.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8.09\u0026thinsp;\u0026plusmn;\u0026thinsp;1.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8.10\u0026thinsp;\u0026plusmn;\u0026thinsp;1.23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.931\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePhosphorus\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4.40\u0026thinsp;\u0026plusmn;\u0026thinsp;1.39\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4.82\u0026thinsp;\u0026plusmn;\u0026thinsp;1.45\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4.68\u0026thinsp;\u0026plusmn;\u0026thinsp;1.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.349\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVitamin D\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e30.47\u0026thinsp;\u0026plusmn;\u0026thinsp;2.75\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e28.30\u0026thinsp;\u0026plusmn;\u0026thinsp;1.58\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e32.40\u0026thinsp;\u0026plusmn;\u0026thinsp;4.70\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.002*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eiPTH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e220.12\u0026thinsp;\u0026plusmn;\u0026thinsp;35.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e219.23\u0026thinsp;\u0026plusmn;\u0026thinsp;34.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e221\u0026thinsp;\u0026plusmn;\u0026thinsp;35.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.635\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFBS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e93.17\u0026thinsp;\u0026plusmn;\u0026thinsp;2.12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e93.90\u0026thinsp;\u0026plusmn;\u0026thinsp;2.35\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e92.44\u0026thinsp;\u0026plusmn;\u0026thinsp;1.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.535\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHBA1C\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.31\u0026thinsp;\u0026plusmn;\u0026thinsp;3.36\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.16\u0026thinsp;\u0026plusmn;\u0026thinsp;3.27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.45\u0026thinsp;\u0026plusmn;\u0026thinsp;3.44\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.411\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCholesterol\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e145.68\u0026thinsp;\u0026plusmn;\u0026thinsp;7.82\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e145.69\u0026thinsp;\u0026plusmn;\u0026thinsp;7.82\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e145.70\u0026thinsp;\u0026plusmn;\u0026thinsp;6.87\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.998\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eAnthropometric Parameters\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMUAC\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.59\u0026thinsp;\u0026plusmn;\u0026thinsp;3.58\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24.31\u0026thinsp;\u0026plusmn;\u0026thinsp;3.15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24.84\u0026thinsp;\u0026plusmn;\u0026thinsp;3.92\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.143\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTTF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e26.62\u0026thinsp;\u0026plusmn;\u0026thinsp;3.49\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.52\u0026thinsp;\u0026plusmn;\u0026thinsp;3.46\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.72\u0026thinsp;\u0026plusmn;\u0026thinsp;3.52\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.560\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMAMC\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.54\u0026thinsp;\u0026plusmn;\u0026thinsp;3.59\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.39\u0026thinsp;\u0026plusmn;\u0026thinsp;3.21\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.67\u0026thinsp;\u0026plusmn;\u0026thinsp;3.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.438\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eBioimpedance Assay\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLTM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e30.11\u0026thinsp;\u0026plusmn;\u0026thinsp;01.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e27.74\u0026thinsp;\u0026plusmn;\u0026thinsp;5.18\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e32.64\u0026thinsp;\u0026plusmn;\u0026thinsp;2.54\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.042*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLTI\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e18.15\u0026thinsp;\u0026plusmn;\u0026thinsp;06.34\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17.07\u0026thinsp;\u0026plusmn;\u0026thinsp;6.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.30\u0026thinsp;\u0026plusmn;\u0026thinsp;2.31\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.237\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFFM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15.33\u0026thinsp;\u0026plusmn;\u0026thinsp;01.04\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.95\u0026thinsp;\u0026plusmn;\u0026thinsp;0.25\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16.49\u0026thinsp;\u0026plusmn;\u0026thinsp;1.57\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.049*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eATM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10.83\u0026thinsp;\u0026plusmn;\u0026thinsp;0.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10.31\u0026thinsp;\u0026plusmn;\u0026thinsp;1.27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e11.30\u0026thinsp;\u0026plusmn;\u0026thinsp;0.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.408\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFTI\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e18.34\u0026thinsp;\u0026plusmn;\u0026thinsp;12.95\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17.39\u0026thinsp;\u0026plusmn;\u0026thinsp;1.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.21\u0026thinsp;\u0026plusmn;\u0026thinsp;2.86\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.230\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eASM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.82\u0026thinsp;\u0026plusmn;\u0026thinsp;3.14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.47\u0026thinsp;\u0026plusmn;\u0026thinsp;3.09\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14.17\u0026thinsp;\u0026plusmn;\u0026thinsp;3.18\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.035*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTBW\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.92\u0026thinsp;\u0026plusmn;\u0026thinsp;5.37\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.39\u0026thinsp;\u0026plusmn;\u0026thinsp;5.41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e26.44\u0026thinsp;\u0026plusmn;\u0026thinsp;5.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.051\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.60\u0026thinsp;\u0026plusmn;\u0026thinsp;2.59\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.63\u0026thinsp;\u0026plusmn;\u0026thinsp;2.41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.56\u0026thinsp;\u0026plusmn;\u0026thinsp;2.77\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.787\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDry weight\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e50.74\u0026thinsp;\u0026plusmn;\u0026thinsp;1.61\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e51.14\u0026thinsp;\u0026plusmn;\u0026thinsp;1.16\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e50.34\u0026thinsp;\u0026plusmn;\u0026thinsp;1.06\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.451\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eSarcopenic parameters\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHand grip\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e18.69\u0026thinsp;\u0026plusmn;\u0026thinsp;3.80\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17.89\u0026thinsp;\u0026plusmn;\u0026thinsp;3.50\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.89\u0026thinsp;\u0026plusmn;\u0026thinsp;3.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.00*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eASMI\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.24\u0026thinsp;\u0026plusmn;\u0026thinsp;1.53\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.00\u0026thinsp;\u0026plusmn;\u0026thinsp;1.37\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.48\u0026thinsp;\u0026plusmn;\u0026thinsp;1.68\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e.002*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003eFOOTNOTES- Baseline demographic, clinical, biochemical, anthropometric, and bioimpedance parameters were compared between sarcopenic and non-sarcopenic CKD patients. Continuous variables are presented as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation; categorical variables as n (%). Group comparisons were performed using independent t-test for continuous variables and chi-square test for categorical variables. p\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant.\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003cp\u003eBMI- Body mass index, CAD- coronary artery disease, DKD- Diabetic kidney disease, CGN- Chronic glomerulonephritis, CTID- chronic tubulointerstitial nephritis, ADPKD- autosomal dominant polycystic kidney disease, HD- Hemodialysis, AVF \u0026ndash; arteriovenous fistula, Hb Haemoglobin, SGOT \u0026ndash; serum glutamate oxaloacetic transaminase, SGPT - serum glutamate pyruvic transaminase, ALP- alkaline phosphatase, iPTH- intact parathyroid hormone, FBS- fasting blood glucose, HBA1C \u0026ndash; glycated haemoglobin, HDL- high density lipoprotein, LDL- Low density lipoprotein, VLDL- very low-density lipoprotein, TG- triglyceride.\u003c/p\u003e\n \u003cp\u003eMUAC: mid-upper arm circumference; MAMC: mid-arm muscle circumference; TTF: triceps skinfold thickness; LTM: lean tissue mass; LTI: lean tissue index; FFM: fat-free mass; ATM: adipose tissue mass; FTI: fat tissue index; ASM: appendicular skeletal muscle mass; TBW: total body water; OH: overhydration.\u003c/p\u003e\n\u003c/div\u003e\n\u003ch3\u003eB. Effect of cholecalciferol supplementation on sarcopenia\u003c/h3\u003e\n\u003cp\u003eCholecalciferol supplementation led to significant functional recovery \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAt three months, 13.2% of confirmed sarcopenia patients fully recovered (p\u0026thinsp;=\u0026thinsp;0.001), and 5.4% improved to probable sarcopenia. At six months, 23.3% fully recovered, and 13.3% moved to the probable category (p\u0026thinsp;=\u0026thinsp;0.001) \u003cstrong\u003e(\u003c/strong\u003eTable \u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e \u003cstrong\u003eand Figure supplementary SF1).\u003c/strong\u003e\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab3\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eSarcopenia improvement and persistence at 3 month and 6 months after cholecalciferol supplementation\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eFollow-Up Period\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003cp\u003eFollowed Up\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eSarcopenic Patients\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eProbable sarcopenia\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eImproved sarcopenia\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eAt 3-Month Follow-Up\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e129\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e105 (81.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e7(5.42%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17(13.17%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.001**\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eAt 6-Month Follow-Up\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e120\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e76(63.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e16(13.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e28(23.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.001**\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\"\u003eFOOTNOTES- Table depicts the change in sarcopenia status at 3-month and 6-month follow-up after cholecalciferol supplementation in CKD stage 5 patients. Values are presented as n (%). \u003cem\u003eProbable sarcopenia\u003c/em\u003e was defined as reduced handgrip strength according to AWGS 2019 criteria, \u003cem\u003eimproved sarcopenia\u003c/em\u003e was defined as meeting higher muscle strength and/or muscle mass thresholds at follow-up compared to baseline. P values represent within-group change over time, calculated using the chi-square test. p\u0026thinsp;\u0026lt;\u0026thinsp;0.05 indicates statistically significant improvement. At 3rd month follow up, 5 patients loss to follow up and at 6th month 9 patients lost to follow up. Analysis was done as per protocol analysis.\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\n \u003cp\u003eFigure shows percentage distribution of sarcopenia classifications at baseline, 3-month, and 6-month follow-up. Blue: sarcopenic patients, Green: probable sarcopenia, Red: improved sarcopenia. Baseline n\u0026thinsp;=\u0026thinsp;134, 6-month n\u0026thinsp;=\u0026thinsp;120. P\u0026thinsp;\u0026lt;\u0026thinsp;0.001.\u003c/p\u003e\n \u003cp\u003eAmong severe cases, 30.8% improved their gait speed by three months (p\u0026thinsp;=\u0026thinsp;0.05), with improvements in 79.8% at six months (p\u0026thinsp;=\u0026thinsp;0.004). ASMI improved progressively, handgrip strength increased by month 3 and plateaued, and gait speed nearly doubled. BMI, MUAC, MAMC, and TTF all increased significantly over six months \u003cstrong\u003e(supplementary table S1 and figure SF2).\u003c/strong\u003e\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\n \u003cdiv align=\"left\" class=\"colspec\"\u003eLine graphs represent the mean values of each outcome parameter (ASMI, Handgrip, Gait Speed, BMI, MUAC, MAMC, TTF) at baseline, 3 months, and 6 months. Shaded regions indicate approximate variability around the mean (based on hypothetical standard deviations for visual illustration). Actual p-values are derived from repeated measures ANOVA and post hoc comparisons.\u003c/div\u003e\n \u003c/div\u003e\n \u003cp\u003eMean vitamin D levels rose from 21.76\u0026thinsp;\u0026plusmn;\u0026thinsp;13.91 ng/mL at baseline to 38.62\u0026thinsp;\u0026plusmn;\u0026thinsp;12.94 ng/mL at 3 months (p\u0026thinsp;\u0026lt;\u0026thinsp;0.0001) and 44.72\u0026thinsp;\u0026plusmn;\u0026thinsp;13.35 ng/mL at 6 months (p\u0026thinsp;\u0026lt;\u0026thinsp;0.01). Vitamin D Deficiency rates dropped from 80.6\u0026ndash;23.5% and 16.4% at 3 and 6 months, respectively in improved sarcopenic patients \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e No cases of hypervitaminosis D (\u0026gt;\u0026thinsp;80 ng/mL), hypercalcemia, hyperphosphatemia, or suppressed iPTH were observed.At 6 months, 83.6% of responder patients were vitamin D sufficient, while 43.5% non-responders remained deficient, suggesting persistent deficiency may contribute to therapeutic failure. Among the responders, it was found that baseline demographics (age, gender, hypertensionand CAD) were similar as non-responders. However, non-responders had significantly higher prevalence of diabetes (66% vs. 34%, p\u0026thinsp;=\u0026thinsp;0.014) whereas responders had higher baseline handgrip strength (19.2 vs. 15.9 kg, p\u0026thinsp;=\u0026thinsp;0.008) and ASMI (5.82 vs. 4.90 kg/m\u0026sup2;, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001), with greater improvements at follow-up in both handgrip and ASMI (p\u0026thinsp;\u0026lt;\u0026thinsp;0.001) \u003cstrong\u003e(\u003c/strong\u003eTable\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab5\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eComparison of Clinical and Hormonal parameters Between Responders and Non-Responders among Sarcopenia Patients\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eParameter\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eResponder (Mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD) n\u0026thinsp;=\u0026thinsp;28\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eNon-Responder (Mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD) n\u0026thinsp;=\u0026thinsp;92\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge (years)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e42.3\u0026thinsp;\u0026plusmn;\u0026thinsp;8.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e43.1\u0026thinsp;\u0026plusmn;\u0026thinsp;9.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.721\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eHypertension, n (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e27 (97.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e81 (88.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.195\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eDiabetes, n (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e18 (64.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e75 (81.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.014\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCAD, n (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1 (3.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8 (8.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.367\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eGender (Male) n (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e22 (78.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e67 ( 72.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.807\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eHANDGRIPV1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19.17\u0026thinsp;\u0026plusmn;\u0026thinsp;1.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15.93\u0026thinsp;\u0026plusmn;\u0026thinsp;1.41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.008\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eHANDGRIPV3\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e26.62\u0026thinsp;\u0026plusmn;\u0026thinsp;1.70\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e18.53\u0026thinsp;\u0026plusmn;\u0026thinsp;1.81\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.00*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eASMI1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.82\u0026thinsp;\u0026plusmn;\u0026thinsp;0.85\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4.90\u0026thinsp;\u0026plusmn;\u0026thinsp;0.83\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.00*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eASMI3\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.05\u0026thinsp;\u0026plusmn;\u0026thinsp;0.79\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.69\u0026thinsp;\u0026plusmn;\u0026thinsp;0.73\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.00*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eTESTOSTERONE\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8.56\u0026thinsp;\u0026plusmn;\u0026thinsp;1.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9.99\u0026thinsp;\u0026plusmn;\u0026thinsp;1.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.645\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eLH\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.30\u0026thinsp;\u0026plusmn;\u0026thinsp;1.84\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10.40\u0026thinsp;\u0026plusmn;\u0026thinsp;1.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.104\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eFSH\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.91\u0026thinsp;\u0026plusmn;\u0026thinsp;2.75\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.74\u0026thinsp;\u0026plusmn;\u0026thinsp;1.49\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.952\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003ePROLACTIN\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e50.30\u0026thinsp;\u0026plusmn;\u0026thinsp;5.83\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e66.87\u0026thinsp;\u0026plusmn;\u0026thinsp;4.82\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.020*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eINSULIN\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10.34\u0026thinsp;\u0026plusmn;\u0026thinsp;1.38\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16.61\u0026thinsp;\u0026plusmn;\u0026thinsp;2.20\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.209\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eHOMA-IR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.01\u0026thinsp;\u0026plusmn;\u0026thinsp;0.07\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4.12\u0026thinsp;\u0026plusmn;\u0026thinsp;0.70\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.004*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eIGF1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e44.80\u0026thinsp;\u0026plusmn;\u0026thinsp;3.30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e30.60\u0026thinsp;\u0026plusmn;\u0026thinsp;4.30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.013*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCORTISOL\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e317.49\u0026thinsp;\u0026plusmn;\u0026thinsp;18.12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e340.34\u0026thinsp;\u0026plusmn;\u0026thinsp;16.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.143\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eT3\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.71\u0026thinsp;\u0026plusmn;\u0026thinsp;0.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.11\u0026thinsp;\u0026plusmn;\u0026thinsp;0.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.032*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eT4\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.47\u0026thinsp;\u0026plusmn;\u0026thinsp;0.90\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.35\u0026thinsp;\u0026plusmn;\u0026thinsp;0.73\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.434\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eTSH\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6.97\u0026thinsp;\u0026plusmn;\u0026thinsp;0.84\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.97\u0026thinsp;\u0026plusmn;\u0026thinsp;0.28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.419\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eiPTH\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e275.93\u0026thinsp;\u0026plusmn;\u0026thinsp;14.14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e190.12\u0026thinsp;\u0026plusmn;\u0026thinsp;27.28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.202\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eVit.D1\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e22.40\u0026thinsp;\u0026plusmn;\u0026thinsp;4.19\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17.89\u0026thinsp;\u0026plusmn;\u0026thinsp;3.07\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.001*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eVit.D3\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e44.31\u0026thinsp;\u0026plusmn;\u0026thinsp;4.47\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e26.85\u0026thinsp;\u0026plusmn;\u0026thinsp;3.07\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.001*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eFOOTNOTES- Continuous variables are expressed as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD; categorical variables as n (%). Comparisons between responders and non-responders were made using independent t-test or chi-square test. HANDGRIP1 and ASMI1 refer to baseline handgrip strength and appendicular skeletal muscle index, respectively; HANDGRIP3 and ASMI3 represent values at 6 months. Vit.D1 and Vit.D3 indicate baseline and 6-month vitamin D levels, respectively. p\u0026thinsp;\u0026lt;\u0026thinsp;0.05 considered statistically significant. p\u0026thinsp;\u0026lt;\u0026thinsp;0.05* was considered statistically significant.\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003ch3\u003eC. Hormonal Abnormalities in Sarcopenic CKD Patients\u003c/h3\u003e\n\u003cp\u003eAmong sarcopenic patients, IGF-1 deficiency was most common (85%), followed by hyperprolactinemia (68%), subclinical hypothyroidism (56.7%)and insulin resistance (47.5%) \u003cstrong\u003e(\u003c/strong\u003eTable \u003cspan class=\"InternalRef\"\u003e5\u003c/span\u003e\u003cstrong\u003e)\u003c/strong\u003e.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab6\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 5\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eBaseline hormonal abnormalities in sarcopenic patients:\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eHORMONE\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eAbnormality Status\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eN (%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eMean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eReference Range\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTestosterone\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeficiency\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMales \u0026minus;\u0026thinsp;29 (24.2%)\u003c/p\u003e\n \u003cp\u003eFemales \u0026minus;\u0026thinsp;5 (4.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9.62\u0026thinsp;\u0026plusmn;\u0026thinsp;1.55\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMales: 4.56\u0026ndash;28.2 nmol/L\u003c/p\u003e\n \u003cp\u003eFemales: 0.2\u0026ndash;2.67 nmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeficiency\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMales \u0026minus;\u0026thinsp;2 (1.7%)\u003c/p\u003e\n \u003cp\u003eFemales \u0026minus;\u0026thinsp;32 (27.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20.03\u0026thinsp;\u0026plusmn;\u0026thinsp;2.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMales: 1.8\u0026ndash;7.8 m IU/L\u003c/p\u003e\n \u003cp\u003eFemales: 1.3\u0026ndash;23.4 m IU/L\u003c/p\u003e\n \u003cp\u003ePostmenopausal: 21.5\u0026ndash;131 m IU/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFSH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeficiency\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMales \u0026minus;\u0026thinsp;41 (34.2%)\u003c/p\u003e\n \u003cp\u003eFemales \u0026minus;\u0026thinsp;5 (4.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.92\u0026thinsp;\u0026plusmn;\u0026thinsp;4.78\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMales: 1.55\u0026ndash;9.74 m IU/L\u003c/p\u003e\n \u003cp\u003eFemales: 1.3\u0026ndash;23.4 m IU/L\u003c/p\u003e\n \u003cp\u003ePostmenopausal: 21.5\u0026ndash;131 m IU/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eProlactin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eExcess\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e78 (68.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e52.25\u0026thinsp;\u0026plusmn;\u0026thinsp;4.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3\u0026ndash;18.6 ng/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eInsulin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eExcess\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17 (14.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15.02\u0026thinsp;\u0026plusmn;\u0026thinsp;2.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFasting: 0\u0026ndash;24 \u0026micro;IU/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHOMA-IR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHigh Insulin Resistance\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e57 (47.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.84\u0026thinsp;\u0026plusmn;\u0026thinsp;0.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal: \u0026lt; 1.6\u003c/p\u003e\n \u003cp\u003eHigh Resistance: \u0026gt;2.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eIGF-1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeficiency\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e103 (85.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e34.60\u0026thinsp;\u0026plusmn;\u0026thinsp;8.30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e184\u0026ndash;205 ng/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCortisol\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eExcess\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13 (10.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e334.54\u0026thinsp;\u0026plusmn;\u0026thinsp;18.44\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e123\u0026ndash;626 nmol/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eiPTH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eExcess\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e51 (42.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e219.23\u0026thinsp;\u0026plusmn;\u0026thinsp;4.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15\u0026ndash;65 pg/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"5\"\u003e\n \u003cp\u003eThyroid hormone\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eSubclinical Hypothyroid\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e76 (56.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eT3 Normal, T4 Normal, High TSH\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eLow T3 Syndrome\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14 (10.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eLow T3, Normal T4, Normal TSH\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eHypothyroid\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20 (14.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eLow T3, Low T4, High TSH\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eEuthyroid\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14 (10.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eNormal T3, Normal T4, Normal TSH\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eHyperthyroid\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1 (0.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eHigh T3, High T4, Low TSH\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eSick Euthyroid Syndrome\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9 (6.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\" colspan=\"2\"\u003e\n \u003cp\u003eLow/Normal T3, Normal T4, Low/Normal TSH\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003eFOOTNOTES- Hormonal abnormalities were defined using standard reference ranges. Values are shown as n (%) and mean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD. Thyroid dysfunction was classified by T3, T4, and TSH profiles. HOMA-IR\u0026thinsp;\u0026gt;\u0026thinsp;2.5 indicated insulin resistance.Total Testosterone, Luteinizing Hormone (LH), Follicle-Stimulating Hormone (FSH), Prolactin, Insulin, Insulin-like Growth Factor-1 (IGF-1), Cortisol, Triiodothyronine (T3) (Thyroxine (T4), Thyroid-Stimulating Hormone (TSH), Homeostatic Model Assessment of Insulin Resistance (HOMA-IR).\u003c/p\u003e\n\u003cp\u003eNon-responders showed higher prolactin (66.9 vs. 50.3 ng/mL, p\u0026thinsp;=\u0026thinsp;0.020), greater insulin resistance (HOMA-IR 4.12 vs. 3.01, p\u0026thinsp;=\u0026thinsp;0.004), lower T3 (1.11 vs. 2.71, p\u0026thinsp;=\u0026thinsp;0.032), and lower IGF-1 (44.8 vs. 30.6 ng/mL, p\u0026thinsp;=\u0026thinsp;0.013). Vitamin D levels were significantly higher in responders, both at baseline (22.4 vs. 17.9 ng/mL, p\u0026thinsp;=\u0026thinsp;0.001) and after supplementation (44.3 vs. 26.9 ng/mL, p\u0026thinsp;=\u0026thinsp;0.001). Other hormonal parameters including testosterone, LH, FSH, cortisol, T4, TSH, and iPTH showed no significant differences \u003cstrong\u003e(\u003c/strong\u003eTable \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eIn vitamin D deficient non-responders, serum 25(OH)D correlated positively with testosterone (r\u0026thinsp;=\u0026thinsp;0.64, p\u0026thinsp;=\u0026thinsp;0.032) and IGF-1 (r\u0026thinsp;=\u0026thinsp;0.76, p\u0026thinsp;=\u0026thinsp;0.028), and negatively with HOMA-R (r = \u0026minus;\u0026thinsp;0.61, p\u0026thinsp;=\u0026thinsp;0.041). These associations highlight a link between low vitamin D, reduced anabolic hormone levels, and insulin resistance. In contrast, among vitamin D sufficient non-responders, IGF-1 showed a paradoxical negative correlation with vitamin D (r = \u0026minus;\u0026thinsp;0.680, p\u0026thinsp;=\u0026thinsp;0.046), and no other hormonal markers showed significant associations, suggesting persistent endocrine dysfunction despite vitamin D correction. \u003cstrong\u003e(Supplementary table S3).\u003c/strong\u003e\u003c/p\u003e\n\u003ch3\u003eD. Associated Risk Factors for sarcopenia\u003c/h3\u003e\n\u003cp\u003eFor the baseline sarcopenia risk factors, diabetes substantially increased sarcopenia risk and dialysis dependence (OR\u0026thinsp;=\u0026thinsp;4.0, p\u0026thinsp;=\u0026thinsp;0.021). Lower MUAC (OR\u0026thinsp;=\u0026thinsp;1.27, p\u0026thinsp;=\u0026thinsp;0.006), MAMC (OR\u0026thinsp;=\u0026thinsp;1.24, p\u0026thinsp;=\u0026thinsp;0.009), and vitamin D deficiency (OR\u0026thinsp;=\u0026thinsp;1.045, p\u0026thinsp;=\u0026thinsp;0.017) also showed significant associations. In multivariate analysis, only diabetes (OR\u0026thinsp;=\u0026thinsp;9.25, p\u0026thinsp;=\u0026thinsp;0.004) and vitamin D deficiency (OR\u0026thinsp;=\u0026thinsp;1.052, p\u0026thinsp;=\u0026thinsp;0.038) remained independent risk factors \u003cstrong\u003e(supplementary Table 4a).\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOn logistic regression analysis, several clinical, nutritional, and hormonal factors were associated with non-response to vitamin D supplementation in sarcopenic CKD patients. In the multivariate model, diabetes (OR 2.3, p=0.032) and catheter vascular access (OR 2.98, p=0.041) emerged as independent clinical predictors. Among muscle indices, both reduced handgrip strength (OR 3.95, p=0.003) and lower ASMI (OR 3.6, p=0.005) were strongly associated with poor response. Endocrine and metabolic abnormalities including low testosterone (OR 2.98, p=0.008), high prolactin (OR 2.45, p=0.022), increased HOMA-IR (OR 2.36, p=0.027), and low IGF-1 (OR 2.65, p=0.010) also remained significant predictors.(supplementaryTable 4b)\u003c/p\u003e\n\u003cdiv id=\"Sec11\" class=\"Section2\"\u003e\n \u003ch2\u003eE. Changes in Quality of Life After Supplementation\u003c/h2\u003e\n \u003cp\u003eAt six months, cholecalciferol supplementation significantly improved KDQOL-36 scores, both physical (PCS) and mental (MCS) components (Table \u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e). No baseline PCS (p\u0026thinsp;=\u0026thinsp;0.606) or MCS (p\u0026thinsp;=\u0026thinsp;0.189) differences existed between CKD5D and CKD5ND groups, but both improved post-supplementation in line with physical recovery and biochemical normalization\u003cstrong\u003e(\u003c/strong\u003eTable \u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e\u003cstrong\u003e).\u003c/strong\u003e\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab8\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 6\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eMean improvement in KDQOL \u0026minus;\u0026thinsp;36 score from baseline to 6 months in sarcopenic after vitamin D supplementation\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eDialysis Status\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eMeasure\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTimepoint\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eMean\u0026thinsp;\u0026plusmn;\u0026thinsp;SD\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCKD5D\u003c/p\u003e\n \u003cp\u003e=\u0026thinsp;67\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePCS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBaseline\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2455.33\u0026thinsp;\u0026plusmn;\u0026thinsp;602.64\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.05\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2585.58\u0026thinsp;\u0026plusmn;\u0026thinsp;1019.21\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMCS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBaseline\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3401.39\u0026thinsp;\u0026plusmn;\u0026thinsp;528.68\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.05\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3523.69\u0026thinsp;\u0026plusmn;\u0026thinsp;984.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCKD5ND\u003c/p\u003e\n \u003cp\u003e=\u0026thinsp;67\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePCS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBaseline\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2534.75\u0026thinsp;\u0026plusmn;\u0026thinsp;580.54\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.03\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2667.58\u0026thinsp;\u0026plusmn;\u0026thinsp;929.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMCS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBaseline\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3521.44\u0026thinsp;\u0026plusmn;\u0026thinsp;491.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3657.47\u0026thinsp;\u0026plusmn;\u0026thinsp;883.46\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTOTAL\u003c/p\u003e\n \u003cp\u003e=\u0026thinsp;134\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePhysical\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBaseline\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2495.04\u0026thinsp;\u0026plusmn;\u0026thinsp;590.55\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.00\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2626.58\u0026thinsp;\u0026plusmn;\u0026thinsp;972.36\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMental\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBaseline\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3461.42\u0026thinsp;\u0026plusmn;\u0026thinsp;511.63\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.00\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3590.58\u0026thinsp;\u0026plusmn;\u0026thinsp;934.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003eFOOTNOTES- KDQOL-36 scores are reported as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation (SD). PCS\u0026thinsp;=\u0026thinsp;Physical Component Summary; MCS\u0026thinsp;=\u0026thinsp;Mental Component Summary. Within-group comparisons between baseline and 6-month scores were analyzed using paired t-tests. A p-value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant.\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n\u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003e In the absence of specific guidelines by KDIGO or KDOQI on vitamin D supplementation for sarcopenia management, this pragmatic, first-of-its-kind study evaluated sarcopenia prevalence and six months vitamin D supplementation response in CKD5. Study showed, one in three and one in four had sarcopenia and severe sarcopenia respectively, with higher prevalence in dialysis patients. Of them, one-fourth of patients showed significant improvement after vitamin D replacement. Notably, not all patients responded to vitamin D therapy, and non-responders had a higher prevalence of diabetes, elevated hormonal abnormalities, and suboptimal 25(OH)D levels.In persistently vitamin D-deficient non-responders, vitamin D levels positively correlated with IGF-1 and testosterone deficiency and negatively with insulin resistance, hinting at modulation of downstream signalling of these hormones by vitamin D.\u003c/p\u003e\u003cp\u003eRelatively higher prevalence of sarcopenia was observed in our study compared to previous studies that documented sarcopenia prevalence ranging from 20\u0026ndash;31% in CKD5 patients (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e).Unlike previous studies, we excluded participants aged more than sixty years due to high primary sarcopenia prevalence in geriatric populations; however, sarcopenia prevalence remained significantly elevated in our younger cohort(\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). This reflects both our exclusion criteria and early-onset CKD from inadequately controlled hypertension and diabetes mellitus, likely attributable to regional variations, nutritional deficiencies, delayed nephrology referrals, greater comorbidity burden and methodological differences in our cohort (\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). Male predominance matched local registry data and healthcare-seeking trends, possibly due to faster muscle loss in men driven by testosterone deficiency and heightened catabolism despite greater baseline muscle mass (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). Although sarcopenia is most common in diabetic kidney disease, followed by hypertension and CAD, it reflects a bidirectional relationship whereby these conditions contribute to muscle wasting through inflammatory mediators (IL-6, TNF-α), vascular dysfunction, and endocrine disturbances(\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eA significant number of our study cohort demonstrated lower BMI, reflecting underlying malnutrition. However, BMI proves inadequate for assessing CKD patients as fluid retention and altered body composition due to masking of nutritional status(\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e). Paradoxically, a subset exhibited sarcopenic obesity, where excess fat infiltration conceals muscle loss. This is consistent with 'hidden sarcopenia' documented in previous CKD studies (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). Present study has used BIA-based equations for ASMI derivation which is equivalent to gold standard DEXA as validated in dialysis populations (r\u0026sup2; = 0.914) and in non-dialysis populations (r\u0026thinsp;=\u0026thinsp;0.954) (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eOnly a limited number of clinical studies have evaluated the efficacy of native vitamin D (cholecalciferol) in improving muscle strength and performance in CKD-related sarcopenia with inconsistent results due to variable dosing, duration, and formulation in these studies. Among them two randomized trials done by Hewitt et al. (50000 IU/week for 2 months ; n\u0026thinsp;=\u0026thinsp;60) and Marckmann et al. (40,000 IU/month for 8 months; n\u0026thinsp;=\u0026thinsp;52), used cholecalciferol but they failed to demonstrate significant improvements in strength or functional outcomes in dialysis patients despite achieving vitamin D repletion(\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). These results contrast with our study where significant improvement in muscle mass, strength and physical performance was seen. These differences may be due to short term supplementation (2\u0026ndash;3 months) which may be insufficient period to detect musculoskeletal improvements, underpowered, utilised fixed non-individualized dosing and absence of sarcopenia-specific inclusion criteria. However, another long term study like ours with high dose cholecalciferol supplementation protocol(50,000 IU weekly adjust levels as per vitamin D levels at 3rd and 6th month for a total of 1 year in haemodialysis patients to see the effect of vitamin D on handgrip strength but it failed to do show any significant difference(geometric mean grip-strength was 27 kg in both groups).The probable explanation was again it was due to less sample size (n\u0026thinsp;=\u0026thinsp;68) and they supplemented only individuals with baseline vitamin D levels less than 20 ng/ml (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). However, other long-term intervention studies have shown sarcopenia improvement by supplementing calcitriol in haemodialysis patients and peritoneal dialysis patients as larger thigh‐muscle cross‐sectional area (+\u0026thinsp;12%, p\u0026thinsp;\u0026lt;\u0026thinsp;0.05), greater muscle strength and 67% lower risk of deterioration in muscle mass and function respectively(\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). However, they have not used native form of vitamin D and they have not used the established criteria of sarcopenia assessment.\u003c/p\u003e\u003cp\u003eOur findings of positive relationship between vitamin D status and muscle strength in CKD populations were also supported by observational studies previously by showing direct association between serum 25(OH)D levels with upper limb handgrip and lower limb quadriceps strength in vitamin D deficit subjects (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e, \u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). In a previous study it was shown that plateau of handgrip strength was seen after achieving threshold value of 30 ng/ml vitamin D which is similar to our study(\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e). However, in our study in addition to plateaued hand grip strength, muscle mass also improved steadily over six months which might be responsible for sarcopenia improvement. We have also seen vitamin D replacement improves sarcopenia in both vitamin D deficit and sufficient patients without any toxic effects. Our study achieved a level of 44.72\u0026thinsp;\u0026plusmn;\u0026thinsp;13.35 ng/mL which is similar to Jean et al. who after monthly 100,000 Iu cholecalciferol supplementation for 6 months, serum 25OHD levels increased from 26.8 to 40.8\u0026thinsp;\u003cspan type=\"Underline\" class=\"Underline\" name=\"Emphasis\"\u003e\u0026plusmn;\u003c/span\u003e\u0026thinsp;9.6 ng/ml nmol/L after 6 months, which is far below the toxicity levels (80 ng/ml)(\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eBeyond vitamin D deficiency, various endocrine imbalances involving anabolic and catabolic hormones have been implicated in sarcopenia. Our study conducted a comprehensive and analysis of nine different hormones to examine their role in sarcopenic CKD patients especially in vitamin D treatment non responsive sarcopenic patients.Aligning with our study of higher prevalence of hypogonadism in both in haemodialysis and non-dialysis males subjects, however a Turkish study has shown a higher prevalence in haemodialysis subjects only (\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e). In our cohort of sarcopenic patients, we have observed lower mean testosterone and gonadotropins levels both in males and females. Our findings align previous trials who have shown a negative correlation between endogenous testosterone levels and gonadotropin levels with worsening CKD stages(\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e). Gonadotropin deficiencies were observed in a sex-specific pattern. LH and FSH suppression were more prominent in females mirroring previous reports of uremic-induced hypothalamic\u0026ndash;pituitary axis disruption more in females (\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e) .\u003c/p\u003e\u003cp\u003eSimilar to the standard thyroid abnormalities in CKD patients, we also found subclinical hypothyroidism (50%) followed by low T3 syndrome (10%) in our patients. Abhilash et al., also found the similar thyroid abnormality aligning to ours (\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e). Hyperprolactinemia was identified in one in seventh patient of our cohort, consistent with previous data reporting prolactin excess in 60% -70% of patients on maintenance dialysis attributable to both reduced renal clearance and increased pituitary secretion, with adverse effects on gonadal function and subsequently muscle health (\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eIGF-1 deficiency emerged as the most prevalent hormonal abnormality in our cohort, affecting 85.8% of patients, consistent with an Indonesian study of elderly dialysis patients with sarcopenia, where IGF-1 suppression was similarly prominent and mean IGF-1 level in our population (34.60\u0026thinsp;\u0026plusmn;\u0026thinsp;68.30 ng/mL) closely matched that of their sarcopenic subgroup (33.43 ng/mL)(\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e). However, our cohort was younger (\u0026lt;\u0026thinsp;60 years), and the prevalence of sarcopenia among dialysis patients was lower (34.7% vs. 82.5%), likely reflecting both age-related differences in IGF-1 levels and the progressive decline in IGF-1 following dialysis initiationas demonstrated in earlier studies reporting up to a 33% reduction in IGF-1 levels after the onset of dialysis.\u003c/p\u003e\u003cp\u003eWe have observed that almost half of the sarcopenic patients had high insulin resistance with HOMA-IR of 3.84 against cutoff value of \u0026gt;\u0026thinsp;2.5, based on a study done by Li et al (\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e).This is aligning with a prior studyby Srinowati et al. who reported 77.5% prevalence of insulin resistance with elevated HOMA-IR of 2.29 against to their lower cutoff of \u0026gt;\u0026thinsp;1.56among elderly haemodialysis patients(\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eDespite achieving sufficient vitamin D levels after six months of supplementation, nearly half of the non-responders showed no improvement, likely due to persistent hormonal abnormalities. IGF-1 deficiency, testosterone deficiency, and insulin resistance were significantly associated with poor treatment response. Among vitamin D\u0026ndash;deficient non-responders, lower vitamin D levels correlated positively with IGF-1 and testosterone deficiency, and negatively with insulin resistance, suggesting a key hormonal influence on treatment failure.\u003c/p\u003e\u003cp\u003eWhile the direct link between vitamin D, testosterone, and sarcopenia in CKD is not fully established, it is plausible that vitamin D deficiency may negatively impact testosterone production or its effects on muscle, exacerbating sarcopenia. Some research suggests that testosterone may enhance the effects of vitamin D on muscle strength as shown in recent meta-analysis of 15 non- CKD studies. They confirmed that vitamin D supplementation significantly increases total testosterone levels, particularly with durations exceeding 12 weeks and dosages above 4000 IU/day(\u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e). The proposed mechanism suggested involves vitamin D receptors and metabolizing enzymes expressed in Leydig cells of the testis, where vitamin D can directly influence testosterone production in human testicular cell cultures as shown in a castrated mice model(\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eOur study reveals a critical biphasic vitamin D\u0026ndash;IGF-1 relationship in sarcopenic patients, with a positive correlation in vitamin D\u0026ndash;deficient non-responders and negative correlation in vitamin D\u0026ndash;sufficient non-responders. This finding aligns with Li \u0026amp; Yu\u0026rsquo;s NHANES III analysis demonstrating a positive correlation below 75 nmol/L (β\u0026thinsp;=\u0026thinsp;0.16, p\u0026thinsp;=\u0026thinsp;0.0103) but negative correlation above this threshold (β = \u0026minus;0.53, p\u0026thinsp;=\u0026thinsp;0.0057) (\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e)Another showed IGF-1 plateauing at 75\u0026ndash;85 nmol/L with reduced metabolic efficacy thereafter (\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e). Mendelian randomization confirms a bidirectional causal relationship, with IGF-1 stimulating 1-α-hydroxylase and vitamin D receptors enhancing IGF-1 concentrations (\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e). Probable mechanisms for the deficient non-responder positive correlation include less compensatory IGF-1 levels restoring the disrupted axis, downregulated 1-α-hydroxylase activity, and reduced IGF-1 receptor sensitivity in vitamin D\u0026ndash;starved muscle as hypothesised by Vicinanza et al(\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e). Conversely, the sufficient non-responder negative correlation reflects vitamin D\u0026ndash;induced IGF-1 receptor desensitization through VDR overexpression, altered IGF binding protein ratios reducing bioavailable IGF-1, established myostatin elevation in advanced sarcopenia and dose\u0026ndash;duration effects where supplementation\u0026thinsp;\u0026gt;\u0026thinsp;1,000 IU/day for \u0026gt;\u0026thinsp;12 weeks produces negative IGF-1 associations (\u003cspan citationid=\"CR41\" class=\"CitationRef\"\u003e41\u003c/span\u003e). However, Trummer et al.\u0026rsquo;s RCT showed no correlation between baseline IGF-1 and 25(OH)D (r\u0026thinsp;=\u0026thinsp;\u0026minus;\u0026thinsp;0.008, p\u0026thinsp;=\u0026thinsp;0.91) but significant correlation with active 1,25(OH)₂D (r\u0026thinsp;=\u0026thinsp;0.21, p\u0026thinsp;=\u0026thinsp;0.005) but notably they excluded patients with egfr\u0026thinsp;\u0026lt;\u0026thinsp;15 ml/min(\u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e). Our findings support shifting from routine supplementation to precision therapy, targeting 50\u0026ndash;75 nmol/L vitamin D, with IGF-1 as a biomarker and individualized strategies.\u003c/p\u003e\u003cp\u003eAn inverse association between 25(OH)D and insulin resistance mirroring our finding where insulin resistance (QUICKI index) correlated negatively with serum 25(OH)D (\u003cspan citationid=\"CR43\" class=\"CitationRef\"\u003e43\u003c/span\u003e). However, this study was done in early CKD stage unlike our advanced satge. In large NHANES III CKD subanalysis it was reported that participants with both reduced eGFR and lower 25(OH)D independently predicted higher HOMA-IR (\u003cspan citationid=\"CR44\" class=\"CitationRef\"\u003e44\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eAt baseline, KDQOL-36 scores revealed no significant differences in PCS or MCS scores between sarcopenic CKD5D and CKD5ND patients, indicating comparable health-related quality of life (HRQoL). This finding is consistent with Manavalan et al., who identified kidney disease component summary score (KDCS) showed a significant decline (P\u0026thinsp;=\u0026thinsp;0.01) from CKD 3 to CKD 5D whereas MCS and PCS showed a nonsignificant decrease(\u003cspan citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e). Following six months of vitamin D supplementation, both PCS and MCS improved significantly from baseline in our cohort which contrast prior evidence linking vitamin D therapy to improved QoL. like Hewitt et al. and Singer et al. who found no QoL benefit despite correcting severe deficiency over 12 months (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). These discrepancies may reflect heterogeneity in dosing regimens, baseline deficiency severity, and study durations.\u003c/p\u003e\u003cp\u003eThe study novelties include long term vitamin D supplementation, first to comprehensively evaluate nine-hormonal axis,finding causes of vitamin D non-responsiveness, appropriately supplementing in baseline vitamin D sufficient individuals without toxicity and used bedside applicable bioimpedance derived equation for sarcopenia diagnosis. Key limitations include lack of randomisation for vitamin D supplementation, absent nutritional and exercise history, sample size for evaluating the effect of hormones on sarcopenia was limited except vitamin D.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eSarcopenia and vitamin D deficiency are highly prevalent in CKD patients. Longer duration, tailored cholecalciferol therapy improves sarcopenic parameters along with mental and physical components of QoL. Persistent hormonal imbalances like IGF-1 deficiency, testosterone deficiency and insulin resistance may limit full therapeutic efficacy of vitamin D among non-responders. These findings highlightthe need for future multidisciplinary approach integrating vitamin D with hormonal association, nutritional support, and physical rehabilitation to effectively counteract sarcopenia in this vulnerable population.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eCKD\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003echronic kidney disease\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eBMI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eBody Mass Index\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eDEXA\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eDual\u0026ndash;Energy X\u0026ndash;ray Absorptiometry\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eCT\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eComputed Tomography\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eMRI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eMagnetic Resonance Imaging\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eBIA\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eBioelectrical Impedance Analysis\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eIGF\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003cb\u003e1\u003c/b\u003e\u0026ndash;Insulin\u0026ndash;like Growth Factor 1\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003ePTH\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eParathyroid Hormone\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eVDR\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eVitamin D Receptor\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eAWGS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eAsian Working Group for Sarcopenia\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eASMI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eAppendicular Skeletal Muscle Index\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eMUAC\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eMid\u0026ndash;Upper Arm Circumference\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eTFF\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eTriceps Fat Fold\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eMAMC\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eMid\u0026ndash;Arm Muscle Circumference\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eESRD\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eEnd\u0026ndash;Stage Renal Disease\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eANOVA\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eAnalysis of Variance\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eASM\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eAppendicular Skeletal Muscle Mass\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eEDTA\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eEthylenediaminetetraacetic Acid\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003e25(OH)D\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e25\u0026ndash;hydroxyvitamin D\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eLH\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eLuteinizing Hormone\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eFSH\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eFollicle\u0026ndash;Stimulating Hormone\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eiPTH\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eIntact Parathyroid Hormone\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eT3\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eTriiodothyronine\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eT4\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eThyroxine\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eTSH\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eThyroid\u0026ndash;Stimulating Hormone\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eELISA\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eEnzyme\u0026ndash;Linked Immunosorbent Assay\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eKDQOL\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003cb\u003e36\u003c/b\u003e\u0026ndash;Kidney Disease Quality of Life\u0026ndash;36 Questionnaire\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eSF\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003cb\u003e12\u003c/b\u003e\u0026ndash;Short Form\u0026ndash;12 Questionnaire\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003ePCS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ePhysical Component Summary\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eMCS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eMental Component Summary\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eIBM SPSS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eInternational Business Machines Statistical Package for the Social Sciences\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eCAD\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ecoronary artery disease\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eAV fistula\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eArteriovenous Fistula\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eHOMA\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003cb\u003eR / HOMA\u003c/b\u003e\u0026ndash;\u003cb\u003eIR\u003c/b\u003e\u0026ndash;Homeostasis Model Assessment of Insulin Resistance\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eKDIGO\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eKidney Disease Improving Global Outcomes\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eKDOQI\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eKidney Disease Outcomes Quality Initiative\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eIL\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003cb\u003e6\u003c/b\u003e\u0026ndash;Interleukin\u0026ndash;6\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eTNF\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003cb\u003eα\u003c/b\u003e\u0026ndash;Tumor Necrosis Factor\u0026ndash;alpha\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003er\u0026sup2;\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eCoefficient of Determination\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eRCT\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eRandomized Controlled Trial\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eeGFR\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eEstimated Glomerular Filtration Rate\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eNHANES\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eNational Health and Nutrition Examination Survey\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eHRQoL\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eHealth\u0026ndash;Related Quality of Life\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u0026bull; \u003cb\u003eKDCS\u003c/b\u003e\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eKidney Disease Component Summary\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate:\u0026nbsp;\u003c/strong\u003eEthical Committee clearance from institutional committee of ABVIMs, Dr. R.M.L. Hospital vide number F.No TP(DM/Mch) 31/2023/IEC/ABVIMS/1406 dated 3\u003csup\u003erd\u003c/sup\u003e August 2023.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eThis study was conducted in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Declaration of Helsinki and its later amendments or comparable ethical standards.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;Trial Registery- Clinical Trial Registery (India) CTRI – CTRI/2025/08/092512 – \u003cstrong\u003eDATED 6\u003csup\u003eTH\u003c/sup\u003e AUGUST 2025( retrospectively enrolled)\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was acquired from the participants prior to their inclusion in the study. All methods were carried out in accordance with relevant guidelines and protocols.\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eConsent for publication: Not applicable\u003c/li\u003e\n \u003cli\u003eAvailability of data and materials: yes data will be shared when asked\u003c/li\u003e\n \u003cli\u003eCompeting interests: we have no competing interest.\u003c/li\u003e\n \u003cli\u003eFunding: not applicable\u003c/li\u003e\n\u003c/ul\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eAuthors' contributions:\u0026nbsp;\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor I: Dr. Disha Arora: Conceptualization\u003c/strong\u003e, Formal analysis, Writing - Original Draft. \u003cstrong\u003eAuthor II:Dr. Lalit Pursnani: \u0026nbsp;\u003c/strong\u003eMethodology, Validation, Formal analysis, Data Curation.\u003cstrong\u003e\u0026nbsp;Author III: Dr. Himansu Sekhar Mahapatra: : I\u003c/strong\u003envestigation, Resources, Writing - Review\u0026amp; Editing. (CORRESPONDING AUTHOR)\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor IV\u003c/strong\u003e: Dr. \u003cstrong\u003eMuthuKumar Balakrishnan:\u003c/strong\u003e Supervision, Project administration, Critical revision of the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;Author V: Dr. Renju Binoy:\u0026nbsp;\u003c/strong\u003ePatient recruitment, Clinical data acquisition, Investigation.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor VI: Dr. Lokesh Kumar Sharma:\u0026nbsp;\u003c/strong\u003eBiochemical analysis, Data interpretation, Validation.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eOther authors: Dr. Hari, Dr. Varuna, and Dr. Vipin:\u0026nbsp;\u003c/strong\u003ePatient management, Data collection, Resources\u003cstrong\u003e. Dr. Lakshman and Dr. Chandra Krishnan:\u0026nbsp;\u003c/strong\u003eStatistical analysis.\u003c/p\u003e\n\u003cp\u003eAcknowledgements:\u0026nbsp;Professor Venkateshan Sekhar, management consultant for helping in statistical analysis. Mr. Sourabh and Miss Deepshikha for helping in Quality-of-life survey and drug adherence follow up.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eDuarte MP, Almeida LS, Neri SGR, Oliveira JS, Wilkinson TJ, Ribeiro HS, et al. Prevalence of sarcopenia in patients with chronic kidney disease: a global systematic review and meta-analysis. Journal of Cachexia, Sarcopenia and Muscle. Volume 15. John Wiley and Sons Inc; 2024. pp. 501\u0026ndash;12.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBellafronte NT, Sizoto GR, Vega-Piris L, Chiarello PG, Cuadrado GB. Bed-side measures for diagnosis of low muscle mass, sarcopenia, obesity, and sarcopenic obesity in patients with chronic kidney disease under non-dialysis-dependent, dialysis dependent and kidney transplant therapy. PLoS ONE. 2020;15(11 November).\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGungor O, Ulu S, Hasbal NB, Anker SD, Kalantar-Zadeh K. Effects of hormonal changes on sarcopenia in chronic kidney disease: where are we now and what can we do? Journal of Cachexia, Sarcopenia and Muscle. Volume 12. John Wiley and Sons Inc; 2021. pp. 1380\u0026ndash;92.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMarckmann P, Agerskov H, Thineshkumar S, Bladbjerg EM, Sidelmann JJ, Jespersen J et al. Randomized controlled trial of cholecalciferol supplementation in chronic kidney disease patients with hypovitaminosis D. Nephrology Dialysis Transplantation. 2012 Sept;27(9):3523\u0026ndash;31.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHewitt NA, O\u0026rsquo;Connor AA, O\u0026rsquo;Shaughnessy DV, Elder GJ. Effects of cholecalciferol on functional, biochemical, vascular, and quality of life outcomes in hemodialysis patients. Clin J Am Soc Nephrol. 2013 July;8(7):1143\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSinger R, Chacko B, Talaulikar G, Karpe K, Walters G. Placebo-controlled, randomized clinical trial of high-dose cholecalciferol in renal dialysis patients: effect on muscle strength and quality of life. Clin Kidney J. 2018;12(2):281\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMolina P, Carrero JJ, Bover J, Chauveau P, Mazzaferro S, Torres PU, Vitamin D. a modulator of musculoskeletal health in chronic kidney disease. Journal of Cachexia, Sarcopenia and Muscle. Volume 8. Wiley Blackwell; 2017. pp. 686\u0026ndash;701.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChen LK, Woo J, Assantachai P, Auyeung TW, Chou MY, Iijima K, et al. Asian Working Group for Sarcopenia: 2019 Consensus Update on Sarcopenia Diagnosis and Treatment. J Am Med Dir Assoc. 2020;21:300\u0026ndash;e3072.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eWang L, Zhu B, Xue C, Zhou F, Luo Q. Lower risk of the deterioration of muscle mass and function in oral active vitamin D users among Incident peritoneal dialysis patients: a 12-month follow-up cohort study. Sci Rep. 2024;14:23951.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGharahdaghi N, Phillips BE, Szewczyk NJ, Smith K, Wilkinson DJ, Atherton PJ. Links Between Testosterone, Oestrogen, and the Growth Hormone/Insulin-Like Growth Factor Axis and Resistance Exercise Muscle Adaptations. Front Physiol. 2020;11:621226.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKatsuhara S, Yokomoto-Umakoshi M, Umakoshi H, Matsuda Y, Iwahashi N, Kaneko H, et al. Impact of Cortisol on Reduction in Muscle Strength and Mass: A Mendelian Randomization Study. J Clin Endocrinol Metab. 2022;107:E1477\u0026ndash;87.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eDeger SM, Hewlett JR, Gamboa J, Ellis CD, Hung AM, Siew ED, et al. Insulin resistance is a significant determinant of sarcopenia in advanced kidney disease. Am J Physiol - Endocrinol Metabolism. 2018;315:E1108\u0026ndash;20.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLin TY, Wu MY, Chen HS, Hung SC, Lim PS. Development and validation of a multifrequency bioimpedance spectroscopy equation to predict appendicular skeletal muscle mass in hemodialysis patients. Clin Nutr. 2021;40:3288\u0026ndash;95.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHays RD, Kallich JD, Mapes DL. Kidney Disease Quality of Life Short Form (KDQOL-SFtm), Version 1.3: A Manual for Use and Scoring [Internet]. RAND; 1997. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://books.google.co.in/books?id=t4YKAQAAMAAJ\u003c/span\u003e\u003cspan address=\"https://books.google.co.in/books?id=t4YKAQAAMAAJ\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ede Amorim GJ, Calado CKM, de Oliveira BCS, Araujo RPO, Filgueira TO, de Fernandes MS. Sarcopenia in Non-Dialysis Chronic Kidney Disease Patients: Prevalence and Associated Factors. Front Med. 2022;9:854410.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGiglio J, Kamimura MA, Lamarca F, Rodrigues J, Santin F, Avesani CM. Association of Sarcopenia With Nutritional Parameters, Quality of Life, Hospitalization, and Mortality Rates of Elderly Patients on Hemodialysis. J Ren Nutr. 2018;28:197\u0026ndash;207.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKumar V, Yadav AK, Sethi J, Ghosh A, Sahay M, Prasad N, et al. The Indian Chronic Kidney Disease (ICKD) study: baseline characteristics. Clin kidney J. 2022;15:60\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eZahed N, Chehrazi S, Falaknasi K. The evaluation of relationship between vitamin D and muscle power by micro manual muscle tester in end-stage renal disease patients. Saudi J kidney Dis transplantation: official publication Saudi Cent Organ Transplantation Saudi Arabia. 2014;25:998\u0026ndash;1003.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChatzipetrou V, B\u0026eacute;gin MJ, Hars M, Trombetti A. Sarcopenia in Chronic Kidney Disease: A Scoping Review of Prevalence, Risk Factors, Association with Outcomes, and Treatment. Calcified Tissue International. Volume 110. Springer; 2022.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eJaffrin MY, Morel H. Body fluid volumes measurements by impedance: A review of bioimpedance spectroscopy (BIS) and bioimpedance analysis (BIA) methods. Med Eng Phys. 2008;30:1257\u0026ndash;69.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRomejko K, Szamotulska K, Rymarz A, Niemczyk S. Muscle Mass and Muscle Strength in Non-Dialysis-Dependent Chronic Kidney Disease Patients. JCM. 2024;13(21):6448.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSinger R, Chacko B, Talaulikar G, Karpe K, Walters G. Placebo-controlled, randomized clinical trial of high-dose cholecalciferol in renal dialysis patients: effect on muscle strength and quality of life. Clin Kidney J. 2019;12(2):281\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGordon PL, Doyle JW, Johansen KL. Association of 1,25-Dihydroxyvitamin D Levels With Physical Performance and Thigh Muscle Cross-sectional Area in Chronic Kidney Disease Stage 3 and 4. J Ren Nutr. 2012 July;22(4):423\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKang SH, Do JY, Cho JH, Jeong HY, Yang DH, Kim JC. Association between Vitamin D Level and Muscle Strength in Patients Undergoing Hemodialysis. Kidney Blood Press Res. 2020;45(3):419\u0026ndash;30.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMori K. Maintenance of skeletal muscle to counteract sarcopenia in patients with advanced chronic kidney disease and especially those undergoing hemodialysis. Volume 13. Nutrients. MDPI AG; 2021.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBataille S, Pedinielli N, Carreno E, Prezelin-Reydit M, Chauveau P, Jean G, et al. VITADIAL Does correction of 25 OH-VITAmin D with cholecalciferol supplementation increase muscle strength in hemoDIALysis patients? study protocol for a randomized controlled trial. Trials. 2021;22(1):364.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eJean G, Souberbielle JC, Lechevallier S, Chazot C. Kinetics of serum 25-hydroxyvitamin D in haemodialysis patients treated with monthly oral cholecalciferol. Clin Kidney J. 2015;8(4):388\u0026ndash;92.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRosas SE, Joffe M, Franklin E, Strom BL, Kotzker W, Brensinger C, et al. Prevalence and determinants of erectile dysfunction in hemodialysis patients. Kidney Int. 2001 June;59(6):2259\u0026ndash;66.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eZitzmann M. Testosterone deficiency and chronic kidney disease. J Clin Translational Endocrinol. 2024 Sept;37:100365.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChang DH, Dumanski SM, Ahmed SB. Female Reproductive and Gynecologic Considerations in Chronic Kidney Disease: Adolescence and Young Adulthood. Kidney Int Rep. 2022;7(2):152\u0026ndash;64.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChandra A. Prevalence of hypothyroidism in patients with chronic kidney disease: a cross-sectional study from North India. Kidney Res Clin Pract. 2016 Sept;35:165\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRojhani E, Rahmati M, Firouzi F, Ziaeefar P, Soudmand SA, Azizi F, et al. Prolactin levels and chronic kidney disease and the subsequent risk of cardiovascular events: A long term population based cohort study. Sci Rep. 2025;15(1):7198.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eWidajanti N, Soelistijo S, Hadi U, Thaha M, Aditiawardana, Widodo et al. Association between Sarcopenia and Insulin-Like Growth Factor-1, Myostatin, and Insulin Resistance in Elderly Patients Undergoing Hemodialysis. Grosset JF, editor. Journal of Aging Research. 2022;2022:1\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLi J, Zhou Q, Liu Z, Zou H. Association of insulin resistance with chronic kidney disease in individuals without diabetes in a community population in South China. BMC Nephrol. 2024;25(1):437.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSrinowati H, Widajanti N, Firdausi H, Thaha M. The Relationship between Insulin Resistance and the Degree of Sarcopenia in Elderly Patients on Maintenance Hemodialysis. J Nat Sc Biol Med. 2021;12:338\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAbu-Zaid A, Saleh SAK, Adly HM, Baradwan S, Alharran AM, Alhatm M et al. The Impact of Vitamin D on Androgens and Anabolic Steroids among Adult Males: A Meta-Analytic Review. Dis 2024 Sept 25;12(10):228.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLi W, Yu T. Relationship between 25-hydroxyvitamin D and IGF1: a cross-sectional study of the Third National Health and Nutrition Examination Survey participants. J Health Popul Nutr. 2023;42(1):35.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHypp\u0026ouml;nen E, Boucher BJ, Berry DJ, Power C, 25-Hydroxyvitamin D. IGF-1, and Metabolic Syndrome at 45 Years of Age. Diabetes. 2008;57(2):298\u0026ndash;305.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eGou Z, Li F, Qiao F, Maimaititusvn G, Liu F. Causal associations between insulin-like growth factor 1 and vitamin D levels: a two-sample bidirectional Mendelian randomization study. Front Nutr. 2023;10:1162442.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eVicinanza R, Frizza A, Pollard JA, Mazza V, De Martino MU, Imbimbo G, et al. Aging and IGF-I: relationships with vitamin D and body composition. A mediation analysis. Front Nutr. 2025 June;24:12:1585696.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRodgers BD, Ward CW. Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs. Endocr Rev. 2022;43(2):329\u0026ndash;65.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eTrummer C, Schwetz V, Pandis M, Gr\u0026uuml;bler M, Verheyen N, Gaksch M et al. Effects of Vitamin D Supplementation on IGF-1 and Calcitriol: A Randomized-Controlled Trial. Nutrients. 2017 June 17;9(6):623.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eŠtef\u0026iacute;kov\u0026aacute; K, Spustov\u0026aacute; V, Krivoš\u0026iacute;kov\u0026aacute; Z, Okša A, Gazd\u0026iacute;kov\u0026aacute; K, Fedelešov\u0026aacute; V et al. Insulin Resistance and Vitamin D Deficiency in Patients With Chronic Kidney Disease Stage 2\u0026ndash;3. Physiol Res. 2011;149\u0026ndash;55.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChonchol M, Scragg R. 25-Hydroxyvitamin D, insulin resistance, and kidney function in the Third National Health and Nutrition Examination Survey. Kidney Int. 2007;71(2):134\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eManavalan M, Majumdar A, Harichandra Kumar K, Priyamvada P. Assessment of health-related quality of life and its determinants in patients with chronic kidney disease. Indian J Nephrol. 2017;27(1):37.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"
[email protected]","identity":"bmc-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bnep","sideBox":"Learn more about [BMC Nephrology](http://bmcnephrol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bnep/default.aspx","title":"BMC Nephrology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Uremic sarcopenia, hormonal relation, cholecalciferol supplementation, chronic kidney disease, quality of life","lastPublishedDoi":"10.21203/rs.3.rs-7434137/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7434137/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eHormonal relationship especially effect of long-term vitamin D supplementation to sarcopenic patients is understudied. This study investigatedassociated risk factors and correlation of different hormones with sarcopenia. Further, effects of six-month cholecalciferol supplementation and quality of life were also studied.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMethodology\u003c/strong\u003e: CKD5 patients aged 18–60 years were screened for sarcopenia using handgrip strength and bioimpedance-based muscle mass. Sarcopenia was classified as probable, confirmed, and severe categories. Confirmed sarcopenic cases were supplemented with 60,000 IU weekly cholecalciferol for 12 weeks in vitamin D deficit and fortnightly for 6 weeks in sufficient patients. Comprehensive nine hormonal profile and risk factor assessment in all sarcopenic patients were done. \u0026nbsp;All were subjected for QoL by KDQOL-36 SF at baseline and 6 months. Changes in Sarcopenia, physical and mental domains of QoL (PCS and MCS) were studied at baseline and 6\u003csup\u003eth\u003c/sup\u003e month.\u003c/p\u003e\n\u003cp\u003eR\u003cstrong\u003eesults\u003c/strong\u003e: Of 401 patients, sarcopenia prevalence as probable, confirmed and severe were 333 (82.29%), 134(33.4%) and 124(25.44%) respectively with higher prevalence in dialysis patients.Vitamin D supplementation showed improvement in confirmed and severe sarcopenia at 3\u003csup\u003erd\u003c/sup\u003e month (13.1 %.and 41.1%) and 6\u003csup\u003eth\u003c/sup\u003e month (23/3% and 66.9%) respectively (p = 0.001). Vitamin D levels deficiency significantly reduced from 80.6% at baseline to 45.5% after supplementation.At six months among non-responder sarcopenic patients exhibited greaterbaseline hormonal abnormalities like high insulin resistance, hyperprolactinemia, lower T3 levels, whereas responder had better baseline muscle strength/mass and higher vitamin D levels. Among non-responder who were still vitamin D deficient showed positive correlation of vitamin D deficiency with IGF-1, testosterone deficiency and negative correlation with insulin resistance was seen. Overall, IGF-1deficiency, insulin resistance,subclinical hypothyroidism, hypogonadism, hyperprolactinemia, were highly prevalent in sarcopenic patients. KDQOL-36 scores improved significantly in mean PCS(p=0.004) and MCS (p = 0.003) after vitamin D supplementation. Diabetes and vitamin D deficiency were determined as risk factor of sarcopenia.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e: Diabetes and vitamin D deficiency are risk factor for sarcopenic CKD5 patients. Six months vitamin D supplementation improved sarcopenia and quality of life in them. Non responsive sarcopenic patients had hormonal imbalances which remain uncorrected or may have blunted therapeutic effects of vitamin D.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTrial registration: \u003c/strong\u003eCTRI/2025/08/092512 –\u003cstrong\u003edated 6\u003c/strong\u003e\u003csup\u003e\u003cstrong\u003eth\u003c/strong\u003e\u003c/sup\u003e\u003cstrong\u003e august 2025\u003c/strong\u003e (retrospectively registered)\u003c/p\u003e","manuscriptTitle":"Relationship of Different Hormone levelsand Effect of six-month Cholecalciferol Supplementationin Sarcopenic End-Stage Kidney Disease: A prospective interventional study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-10-17 15:47:59","doi":"10.21203/rs.3.rs-7434137/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2025-10-17T21:16:38+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"148951171039065863595840695109034388084","date":"2025-10-08T18:19:55+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-10-06T11:58:35+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-09-09T07:52:59+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-08-25T13:25:07+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-08-25T13:24:48+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Nephrology","date":"2025-08-22T11:29:00+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"
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