Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury | 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 Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury Nisha Jose, Sanjeet Roy, Jeethu Joseph Eapen, Athul Thomas, Joseph Johnny, and 5 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4878222/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Introduction: Acute kidney injury (AKI) is no longer considered a single hit disease but part of a spectrum that culminates in adverse renal and cardiovascular outcomes. What are the renal biopsy findings of patient with persistent AKI/AKD (acute kidney disease)? Are there renal biopsy characteristics which predict renal recovery. These are the questions that this study addresses. Methodology: A retrospective study was conducted analyzing all patients who underwent a renal biopsy with a diagnosis of acute kidney injury from January 2021 to January 2023 from the online hospital database. Patients with other glomerular disease and transplant patients were excluded from this cohort. The clinical and renal biopsy characteristics were analyzed for their correlation with renal recovery. Results: Of 420 patients screened, 54 were included in the study. Most patients had stage 3 AKI. The median follow up in this study was 80.50 days. Among those on dialysis, 55.6% of patients became free of KRT (kidney replacement therapy). 92.6% of the study population had diffuse tubular involvement on the renal biopsy. Clinical recovery correlated with the degree of vasculature involvement on the renal biopsy. Interstitial fibrosis and tubular atrophy corelated with progression to CKD. Among the clinical features, the cause of AKI, presence of pre-existing CKD and Charleston co-morbidity score correlated with independence from KRT. Conclusion: Specific findings on the renal biopsy such as atherosclerotic changes correlate negatively with long-term recovery in AKI and renal biopsy findings of interstitial fibrosis and tubular atrophy may help to prognosticate progression to CKD.. Among clinical characteristics, the presence of co-morbidities and pre-existing CKD correlates negatively with renal recovery. Figures Figure 1 Figure 2 Figure 3 Introduction AKI (acute kidney injury) the term provides a convenient label to categorize a heterogenous cluster of illness all of which have differing courses and outcomes. Of the total number of renal biopsies, acute kidney injury occupies 31.7% among hospitalised patients( 1 ). There is an increased risk, about 2–7 fold times, of bleed associated with biopsies in an acute hospitalised setting as opposed to patients undergoing routine out-patient non emergent biopsies( 2 ). The lack of a proper etiological diagnosis for AKI particularly when underlying causes of injury are occult, along with ambiguity on the use of drugs or toxins often forces the clinician to take on the risk of the kidney biopsy. The histopathological findings on a biopsy for acute kidney injury that actually correlate with renal recovery are unknown. This study aims to evaluate the value of the renal biopsy done for AKI in terms of its use in prognostication and renal recovery. Acute kidney injury has evolved from being considered a single hit disease to being a part of a continuum that ultimately results in CKD( 3 ). The etiologies of AKI in the west are very different from those seen in third world countries where snake bite and diarrhoea are still of major concern. Is all AKI similar in its outcome leading to a steady progression to CKD? Is the prognosis same in a younger population with a single event of AKI and no other co-morbidities? Does a renal biopsy done in this setting really prognosticate recovery equally for all etiologies? These are some of the questions this study aims to answer. Methods A retrospective cohort study was conducted in a tertiary level hospital in South India including all patients between the time period of 2021–2023 January with a diagnosis of acute kidney injury who underwent a renal biopsy. Inclusion criteria: Adult patients with a biopsy proven diagnosis of AKI on the kidney biopsy Exclusion criteria Concomitant glomerular disease Transplant patients Children These specific exclusion criteria of transplant and glomerular disease were chosen since in these subsets, the renal recovery may correlate with the specific glomerular pathology such as rejection or treatment of the glomerular disease rather than the AKI alone. In children outcome variables may need to be modified and the etiology of AKI is different than that seen in adults Data was collected from the hospital database. Certain key words were used to identify AKI on the renal biopsy reports: “acute tubular injury, acute tubular necrosis, cortical necrosis, severe tubular injury, diffuse tubular injury”. Patients who had these key words in their biopsy reports, were then screened for their eligibility into the study. Data was analysed for demography, presence and etiology of AKI as per KDIGO criteria, co-morbidities, use of dialysis and recovery parameters, death and recurrence of AKI. Specific outcome parameters were defined. The renal biopsy findings were available on the online database and these were used to correlate with specific parameters of clinical recovery. The renal biopsy data were reviewed by both a nephrologist and trained renal pathologist. Outcome parameters The primary outcome of the study was to evaluate the correlation between the renal biopsy report and recovery from AKI at maximum follow up. Secondary outcomes To identify the recovery rate and follow up rate of patients with acute kidney injury To identify clincial risk factors associated with poor renal recovery and progression to CKD such as age, BMI, presence of co-morbidities, requirement and duration of KRT. Definitions used in this study AKI: As defined by the KDIGO 2012 criteria( 4 ). Refer to supplementary table 4 for criteria for baseline creatinine. Co-morbidities were evaluated using the Charlston co-morbidity( 6 ) and the AKI risk prediction score( 7 ) was also checked for these patients. Renal recovery was defined as follows Complete recovery: Return to baseline creatinine or normal creatinine value Partial recovery: Fall in the stage of AKI Non-resolving AKI: AKI that does not resolve within 72 hours( 8 ) Resolving AKI: resolved within 72 hours MAKE (Major adverse kidney events) events( 9 ) are defined as: either death, new requirement for dialysis or worsening of kidney function denoted by > 25% decline in eGFR from baseline. MAKE events were considered at 30 days, 60 days and 90 days Kellum classification( 10 ) was also used for assessing different types of renal recovery This study was reviewed by the institutional review board of this hospital and approved. The IRB number is IRB Min no15967. Statistical analysis Mean and standard deviation was reported for all the continuous variables following normality and Median and IQR (Inter Quartile Range) was reported for all the continuous variables not following normality. Frequency and percentage were reported for all the categorical variables. The parametric t-test was performed to compare the continuous variables following normality for two groups and Mann-Whitney test was performed to compare the continuous variables not following normality for two groups. Normality of the variable was assessed using rule of thumb. The Pearson Chi-square test was performed to find the association between the categorical variables. The Pie chart was plotted to show that etiology of acute kidney injury and indication for renal biopsy. The bar charts was plotted to show that frequency of outcome measures in AKI, various Kellum classes of AKI and frequency of various biopsy findings in AKI. The p-value less than 0.05 shows the statistical significance. Statistical analysis was performed using Statistical Package for Social Science (SPSS) version 21. 25.0 (IBM statistic, New York, USA). Results The consort diagram of the study (Fig. 1 ) shows that out of 420 patients identified on screening, only 54 were finally included. The majority of patients excluded were patients with concomitant glomerular disease. The patient population consisted of patients with drug or toxin induced AKI (the majority) followed by septic patients and those with snake bite AKI (Table 1 ). The mean age of patients was 44.9 years. Most were of normal BMI and only 61.1% of them had no known co-morbidities. About 70% of this population required dialysis and 96.3% of them had stage 3 AKI. Patient were followed by for a median of 80.50 days. Time to achieve nadir creatinine was 57 days. The mean duration of hospitalisation was 17.87 days. Among those who were on dialysis, the average time spent on dialysis was 21 days and 55.6%% became free of KRT eventually. The most commonly used modality in this study was IHD (intermittent hemodialysis) in 89.47% of patients (Table 2 ). Of the total number of patients, 72.2% of patients had microhematuria and proteinuria was present in 39% of patients. Most of the renal biopsies (76%), were done for an etiological evaluation of renal dysfunction when a clear diagnosis as to the cause of AKI was not present or an alternate etiology like Acute tubule-interstitial diagnosis or rapidly progressive glomerulonephritis was entertained, while 24% were done for prognostication. Table 1 Baseline characteristics on the study population Characteristic Frequency N = 54 Age Mean (Standard Deviation) 44.91 (SD14.04) Gender : Male : female n (%) 34(63%):20(37%) Average BMI Mean (SD) Median (IQR) BMI: underweight : 30kg/m2 22.47 (SD45.83) 21.8 (19.52–23.55) 7 (16.7) 26 (61.9%) 6 (14.3%) 3 (7.1%) Co-morbidities Diabetes Hypertension Pre-existing CKD Chronic liver disease Cardiovascular disease Burns or trauma Major surgery Others 14 (25.9%) 18 (33.3%) 6 (11.1%) (5 stage 3 and 1 stage 4) 3 (5.6%) 0 1 (1.9%) 0 13 (24.07%) Charlston co-morbidity score 0 score – no co-morbids Mild (score 1,2) Moderate (score 3,4) Severe (5 and above) 33 (61.1) 13 (24.1) 4 (7.4) 4 (7.4) Cause of AKI Urinary tract infection Pigment related AKI Poisoning Drug or toxin induced Snake bite AKI Pancreatitis Sepsis Hypovolemia Hypercalcemia Hepato-renal syndrome 1 1 2 19 6 1 13 8 2 1 Stage of AKI Stage 1: Stage 2: Stage 3: 0 2 (3.7%) 52 (96.3%) Requirement of dialysis Yes No 38 (70.4%) 16 (29.6%) Number of patients on mechanical ventilation 8 (14.8%) Number of patients on inotropes 5 (9.3%) AKI risk prediction score Low (0-2.9) Moderate (3-8.9) High (9-11.5) Very high (more than 11.5) 22 (40.7) 30 (55.6) 2 (3.7) Site of admission Outpatient Ward ICU 0 37 (68.5%) 17 (31.5%) Duration of hospitalization Mean (SD) Median (IQR) 17.87 (SD45.22) 10 (5.75–17.25) Mean Admission creatinine 6.65 (5.13) Days to reach maximum creatinine value Mean (SD) Median (IQR) 134.72 (SD188.57) 4 ( 1 – 14 ) Nadir creatinine Mean (SD) Median (IQR) 2.61 (SD2.52) 1.51 (0.93–3.86) Days to reach nadir value of creatinine Mean (SD) Median (IQR) 134.72 (SD188.57) 57 (15.75–177.50) Duration of follow up Mean (SD) Median (IQR) 186.68 (SD249.19) 80.50 (24.50-229.25) Creatinine at maximum follow up Mean (SD) Median (IQR) 3.67 (SD4.49) 1.69 (0.94–5.24) Table 2 Details of the use of dialysis for AKI Characteristic Frequency (percentage) Number of patients on KRT 38 (70.4%) Type of KRT used (n = 38) IHD SLED CRRT (Some patients used multiple modalities) 34 (89.47%) 5 (13.16%) 1 (2.63%) Number of sessions 5.45 Number of days on KRT Mean (SD) Median 22.48 (SD4.83) 21.8 (0–18.00) Number of patients who became free of KRT 30 (55.6%) When looking at various outcome measures of AKI, the incidence of MAKE events at 30 days was found to be 7.4% which decreased to 3.7% at 60 and 90 days (Fig. 2 ). All patients in this cohort had persistent AKI (i.e., persisting beyond 48 hours). Partial recovery was seen in 33.3% and complete recovery in 38.9%. Overall, 72.2% of patients showed some form of renal recovery. Only 1 patient died in this cohort. Most patients (98.1%) had AKD (acute kidney disease) and 44.4% of them were labelled as CKD (chronic kidney disease) subsequently. Most patients were classified as Kellum class 4 i.e., without complete recovery at hospital discharge but showing some form of renal recovery. Among the clinical features, the cause of AKI, presence of pre-existing CKD and Charleston co-morbidity score seemed to correlate negatively with independence from KRT (Table 3 ). Among the laboratory parameters the admission creatinine and maximum creatinine and days taken to reach the nadir correlated negatively with independence from KRT and complete recovery of the renal injury. Presence or absence of AKD did not seem to have any bearing on long term renal recovery of independence from KRT. Table 3 Table representing correlation of various clinical characteristics with outcome measures of AKI Variable P value for partial recovery Complete recovery P value Independence from KRT P Value Transitioned to CKD P value Composite of renal recovery and independence from KRT P value Age 0.201 0.637 0.829 0.715 0.874 Gender 0.84 0.480 0.950 0.553 0.328 BMI 0.432 0.524 0.373 0.324 0.769 Stage of AKI 0.54 0.147 0.193 1 1 Cause of AKI 0.39 0.12 0.38 0.006 0.86 Requirement of KRT 0.14 0.089 < 0.001 0.235 0.734 Co-morbidities Diabetes Hypertension Pre-existing CKD Stage of CKD CLD Burns or trauma Major surgery 0.18 0.54 0.65 0.767 0.25 1 0.418 0.77 0.55 0.386 0.778 1 0.389 0.017 0.890 0.245 0.005 0.005 0.575 1 0.720 0.115 0.051 0.027 0.056 1 0.42 0.012 0.407 0.487 0.018 0.018 1 1 0.356 Charlston co-morbidity score 0.08 0.507 0.005 0.038 0.537 Mechanical ventilation 0.70 1 0.277 1 1 Inotropes requirement 1 0.144 1 0.442 0.306 AKI risk prediction score 1 0.628 0.238 0.273 0.341 Admission creatinine 0.811 0.579 0.009 0.826 0.441 Maximum creatinine 0.970 0.785 0.001 0.411 0.983 Days to reach maximum creatinine value 0.800 0.175 0.841 0.180 0.820 nadir value of creatinine 0.130 < 0.001 0.251 < 0.001 0.002 Days to reach nadir value of creatinine 0.419 0.028 0.009 0.653 < 0.001 Type of KRT used 0.44 0.078 < 0.001 0.126 0.227 Number of sessions 0.428 0.046 < 0.001 0.067 0.880 Number of days on KRT 0.483 0.039 < 0.001 0.062 0.970 Free of KRT 0.004 0.851 ---- 0.609 ----- Kellum class 0.102 < 0.001 < 0.001 0.002 < 0.001 AKD 1 0.389 0.444 0.442 1 The frequency of various biopsy findings in acute kidney injury is presented in Fig. 3 . 92.6% of patients had diffuse involvement of tubules on renal biopsy. Cortical involvement in the form of cortical necrosis was seen in 5.6% of patients. The most frequent finding on the renal biopsy was dilatation of tubules followed by flattening of the tubular lining epithelium. 77.8% of cases the brush border was damaged. Chronic vascular sclerotic changes were present in 61.1% of patients. Interstitial fibrosis and tubular atrophy (IFTA) was present in 50% of patients. The association of diabetes with glomerulosclerosis on the kidney biopsy in this setting was not significant (p value 0.568) however, hypertension was significantly associated with glomerulosclerosis (p value of 0.203). The presence of IFTA was significantly correlated with diabetes (p value 0.295) but not associated with presence of hypertension (p value of 0.614). Vascular changes were not significantly associated with diabetes or hypertension in this setting (p value 0.758 and 0.713 respectively). Pre-exiting CKD was significantly correlated with both presence of glomerulosclerosis, IFTA and atherosclerosis. Severe degrees of glomerular injury are generally absent in cases of acute kidney injury. The only biopsy finding which correlated with independence from KRT was presence of sloughing (Table 4 ). Recovery both complete and partial, had a correlation with presence of chronic vascular sclerotic changes. IFTA correlated with progression to chronic kidney disease. Presence of vacuolization on the renal biopsy correlated with complete recovery. Table 4 Correlation of biopsy findings with various outcome measures in AKI Variable P value for partial recovery Complete recovery P value Independence from KRT p value Transitioned to CKD p value Composite of renal recovery and independence from KRT P value Site of involvement Cortex or Medulla 0.543 0.274 0.579 0.243 0.121 Tubular changes due to AKI Degree of involvement Focal or Diffuse- 1 0.638 1 1 1 Presence of sloughing 1 0.97 0.016 0.728 0.708 Presence of flattening 1.00 1 1 0.618 1 Presence of dilation of tubules 1 0.287 1 1 0.564 Presence of necrosis of tubules 0.30 0.117 0.359 0.152 0.485 Regenerative changes noted on biopsy 1 0.253 0.415 0.373 0.071 Presence of Vacuolization of tubules 0.512 0.028 0.890 0.708 0.261 Loss of brush border 1 0.747 0.272 0.470 0.714 Denudation of the tubular basement membrane 1 0.389 1 0.442 1 Tubular cell calcification 1 0.723 0.165 0.680 1 Interstitial changes due to AKI Interstitial edema 0.846 0.272 0.667 0.388 0.556 IFTA more than 25% 0.634 0.066 0.565 0.008 1 Glomerular changes due to AKI Glomerulosclerosis more than 25% 0.549 0.518 0.677 0.320 0.179 Vascular changes identified Arteriosclerosis 0.016 0.003 0.534 0.027 0.495 Discussion The exact prognostic value of a kidney biopsy in the setting of AKI has not been studied previously. This study looks at both clinical and renal biopsy prognostic variables in renal recovery from AKI in the setting of a developing country where the etiology and setting of AKI is often different from that seen in the developed world. The patient population The transplant and glomerulonephritis cohorts have been included in other research on AKI( 10 ). However, when looking at the pathology of AKI it was essential to exclude these patients since glomerulonephritis cause specific pathological changes in the kidney which might confound the interpretation of the extent of involvement of the acute kidney injury on the renal biopsy. The most common cause of AKI in this cohort was drug or toxin induced acute kidney injury and septic AKI (Table 1 ). In data from the Indian society of nephrology AKI registry, sepsis (34.7%) and tropical fevers (9.8%) were considered to be the most common etiology of community acquired AKI followed by AKI associated with liver disease (9.1%) ( 12 ). Snake bite AKI is also fairly common in these regions. The difference is the etiological diagnosis in this study when compared to others on AKI is likely because only patients who underwent a kidney biopsy were included. The co-morbidity profile (Table 1 ) is similar to that observed in the ISN registry with hypertension being the most common co-morbidity and diabetes following closely. When compared to data from developed nations, it is noted that AKI in the developing world occurs more frequently in younger patients with fewer co-morbidities as opposed to the developed world where older populations with more number of comorbidities develop AKI( 13 ). The cohort in this research study were individuals who had severe AKI, that is most of them required dialysis and more than 95% of them had stage 3 AKI. This data is in keeping with prospective studies done in India where more than 50% of patients have AKI stage 3( 12 , 14 ). Follow up and outcome measures Patients were followed up for a median of 80.50 days (Table 1 ). Data from other studies showed that only about 13-37.3%( 14 ) of patients with AKI remain on follow up with a nephrologist among Medicare patients( 15 ). Follow up needs to be streamlined for better patient outcomes especially in high-risk patients. Traditionally it is considered that recovery from AKI follows 4 steps, initiation, maintenance, polyuria and restitution. Renal recovery is expected to occur within 3 month, if it doesn’t if is labelled CKD( 16 ). In this study however, although most patients who stop dialysis do so over a mean of 22.48 days, recovery takes much longer with nadir creatinine generally being achieved over a period of 57 days or more. This is in keeping with data from the mayo clinic services, most patients were able to discontinue dialysis before 6 months while the remaining recovered over a period of 12 months. This may be an important take home message from this data, that recovery occurs slowly and can be anticipated even after 3 months. A majority (55.6%) of patients on dialysis became free of dialysis during the course of their treatment (Table 2 ). When compared to western data, this number is low in that among 50% of AKD patients who have survived their initial hospitalisation, only 30% generally required continuation of KRT( 17 ). The higher number in this cohort maybe due to the selection bias of patients. Patients who are likely to not recover AKI, were more likely to require kidney biopsies for prognostication or to provide an alternate diagnosis for the kidney injury. The clinical characteristic that correlated with renal recovery and outcome measures such as independence from KRT (Table 3 ) is similar to those documented in another study where underlying CKD and presence of co-morbidities corelate poorly for these measures( 18 ). It is interesting to note that labelling the disease as AKD does not portend a poor prognosis for renal recovery. Another interesting finding is that not just the nadir creatinine that correlates with composite measures of renal recovery but also the time to achieve the nadir. This may give us an early clue likelihood of renal recovery even before nadir creatinine is achieved. The urine sediment Pre-renal AKI is known to have a bland sediment, while in ATN urine may show hematuria and muddy brown casts. Automated analysers are less sensitive and specific to detect these casts when compared with a nephrologist interpretation of the urine sediment( 19 ). In this cohort, automated analysers were used to assess urine and the difficulty is often differentiating a severe AKI which has caused ATN from a glomerular disease. This may be a contributing factor to the number of biopsies that were done in the acute phase of the illness to rule out a glomerular disorder. Outcome measures of AKI When it comes to measuring renal recovery, there is no dearth of outcome measures( 20 ). The myriad different interpretations of renal recovery and measures make comparing data between studies difficult. Some examples of renal recovery measures that are used in various studies are MAKE DC, 30, 60,90 and 1 year events, while others look at partial recovery (defined variably in different studies) vs. complete recovery. Still other studies look at AKI as transient or persistent based on a 48-hour window. To make the results comparable, we looked at all these outcome variables in AKI, MAKE 30 events were very low, as were MAKE 60, and 90 events (Fig. 2 ). In data from another trial the incidence of MAKE is approximately 30%( 21 ). These may represent a selection bias in that only patients who survived this initial episode of AKI and were fit for biopsy were included in this study. However, it should be remembered that, most of this cohort were dialysis requiring AKI and the number of MAKE events is much lower than expected. One possible reason is the etiology of AKI which is different than the west and the lower co-morbidity burden of this population. Kellum et al suggested a novel method of quantifying recovery based on timing and degree of recovery. This classification showed the pattern of renal recovery and in other data proved to predict long term outcomes( 22 ). In this cohort the Kellum classes had good correlation with other measures of renal recovery such as complete recovery and independence from KRT (Table 3 ). Biopsy findings in AKI The relative frequency of biopsy findings is shown in Fig. 3 . In a systematic review of biopsy findings in AKI, A similar pattern to this one was noted by Wen et al( 23 ). As in this study, tubular sloughing was a common finding followed by epithelial cell flattening and simplification. Very little data is available worldwide correlating biopsy findings with clinically significant outcomes for AKI. One such study was a post-mortem analysis of patients who underwent kidney biopsy for acute kidney injury in COVID-19 patients( 24 ). The only histopathological finding that correlated with severity of AKI and recovery was presence of pigmented casts. This study provides new insight and findings into correlation of biopsy findings with renal recovery and independence from KRT. As can be expected, chronic vascular sclerotic changes on the renal biopsy have significant correlation with renal recovery (Table 4 ). This is possibly because the pathophysiology of acute kidney injury is closely linked to renal vasoconstriction, endothelial injury and activation of inflammatory pathways( 25 ). It makes sense that poor blood supply with arteriosclerotic vessels would play an important role in renal recovery. Vacuolisation is commonly seen in drug and toxin induced AKI due to ART (anti-retroviral therapy), CNI (calcineurin inhibitors) and contrast media and hence probably has a specific correlation with etiology and renal recovery( 26 ). Interstitial fibrosis and tubular atrophy in several glomerular diseases has been liked to disease progression( 27 ). This study is a first-of-its-kind cohort study looking at renal biopsy findings and correlating them with renal recovery however, the selection bias of the study, to include only biopsy proven AKI, will limit the generalisability of the data to all AKI. Conclusions Renal recovery occurs slowly with nadir creatinine being achieved over a mean of 57 days. Clinical characteristics associated negatively with independence from KRT include presence of pre-existing CKD and the Charleston comorbidity index. Renal biopsy findings that corelate positively with progression to CKD include presence of interstitial fibrosis and tubular atrophy. Chronic vascular sclerotic changes on a renal biopsy have significant negative correlation with renal recovery. The degree of glomerular damage does not correlate with recovery from AKI. Declarations Disclosure: Dr Jose et al have no conflicts of interest to disclose Funding: No external funding was used for this study Author Contribution NJ, SR, RK, JJ and SSR wrote the main manuscript and prepared figuresATJ, JJE, SV, SA, VGD reviewed and edited the manuscript Acknowledgement I acknowledge Mr Srinivasan statistician working in christian medical college for his help with the statisitics Data sharing: all the data that support the findings is included in the manuscript. References Abuduwupuer Z, Lei Q, Liang S, Xu F, Liang D, Yang X, et al. The Spectrum of Biopsy-Proven Kidney Diseases, Causes, and Renal Outcomes in Acute Kidney Injury Patients. Nephron. 2023;147(9):541–9. Waikar SS, McMahon GM. Expanding the Role for Kidney Biopsies in Acute Kidney Injury. Semin Nephrol. 2018;38(1):12–20. Takaori K, Yanagita M. Insights into the Mechanisms of the Acute Kidney Injury-to-Chronic Kidney Disease Continuum. Nephron. 2016;134(3):172–6. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract. 2012;120(4):c179–184. Charlson ME, Carrozzino D, Guidi J, Patierno C. Charlson Comorbidity Index: A Critical Review of Clinimetric Properties. Psychother Psychosom. 2022;91(1):8–35. Malhotra R, Kashani KB, Macedo E, Kim J, Bouchard J, Wynn S, et al. A risk prediction score for acute kidney injury in the intensive care unit. Nephrol Dial Transpl. 2017;32(5):814–22. Association Between Early Recovery of Kidney Function After Acute Kidney Injury and Long-. term Clinical Outcomes | Nephrology | JAMA Network Open | JAMA Network [Internet]. [cited 2024 Mar 16]. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2764347 Billings FT, Shaw AD. Clinical trial endpoints in acute kidney injury. Nephron Clin Pract. 2014;127(1–4):89–93. Kellum JA, Sileanu FE, Bihorac A, Hoste EAJ, Chawla LS. Recovery after Acute Kidney Injury. Am J Respir Crit Care Med. 2017;195(6):784–91. Abuduwupuer Z, Lei Q, Liang S, Xu F, Liang D, Yang X, et al. The Spectrum of Biopsy-Proven Kidney Diseases, Causes, and Renal Outcomes in Acute Kidney Injury Patients. Nephron. 2023;147(9):541–9. Prasad N, Jaiswal A, Meyyappan J, Gopalakrishnan N, Chaudhary AR, Fernando E et al. Community-acquired acute kidney injury in India: data from ISN-acute kidney injury registry. Lancet Reg Health - Southeast Asia [Internet]. 2024 Feb 1 [cited 2024 Feb 21];21. https://www.thelancet.com/journals/lansea/article/PIIS2772-3682(24)00009-X/fulltext Yang L. Acute Kidney Injury in Asia. Kidney Dis. 2016;2(3):95–102. Priyamvada PS, Jayasurya R, Shankar V, Parameswaran S. Epidemiology and Outcomes of Acute Kidney Injury in Critically Ill: Experience from a Tertiary Care Center. Indian J Nephrol. 2018;28(6):413–20. Wu VC, Chueh JS, Chen L, Huang TM, Lai TS, Wang CY, et al. Nephrologist Follow-Up Care of Patients With Acute Kidney Disease Improves Outcomes: Taiwan Experience. Value Health. 2020;23(9):1225–34. Silver SA, Siew ED. Follow-up Care in Acute Kidney Injury: Lost in Transition. Adv Chronic Kidney Dis. 2017;24(4):246–52. Patschan D, Müller GA. Acute kidney injury. J Inj Violence Res. 2015;7(1):19–26. Clark EG, James MT, Hiremath S, Sood MM, Wald R, Garg AX, et al. Predictive Models for Kidney Recovery and Death in Patients Continuing Dialysis as Outpatients after Starting in Hospital. Clin J Am Soc Nephrol. 2023;18(7):892. Godin M, Macedo E, Mehta RL. Clinical Determinants of Renal Recovery. Nephron Clin Pract. 2014;127(1–4):25–9. Cavanaugh C, Perazella MA. Urine Sediment Examination in the Diagnosis and Management of Kidney Disease: Core Curriculum 2019. Am J Kidney Dis. 2019;73(2):258–72. Kellum JA. How Can We Define Recovery after Acute Kidney Injury? Considerations from Epidemiology and Clinical Trial Design. Nephron Clin Pract. 2014;127(1–4):81–8. Sparks M, Renal Fellow N. 2022 [cited 2024 Feb 28]. Making Sense of Make (Major Adverse Kidney Events) After AKI. https://www.renalfellow.org/2022/10/05/making-sense-of-make-major-adverse-kidney-events-after-aki/ Gameiro J, Marques F, Lopes JA. Long-term consequences of acute kidney injury: a narrative review. Clin Kidney J. 2021;14(3):789–804. Wen Y, Yang C, Menez SP, Rosenberg AZ, Parikh CR. A Systematic Review of Clinical Characteristics and Histologic Descriptions of Acute Tubular Injury. Kidney Int Rep. 2020;5(11):1993–2001. Rivero J, Merino-López M, Olmedo R, Garrido-Roldan R, Moguel B, Rojas G, et al. Association between Postmortem Kidney Biopsy Findings and Acute Kidney Injury from Patients with SARS-CoV-2 (COVID-19). Clin J Am Soc Nephrol CJASN. 2021;16(5):685–93. Makris K, Spanou L. Acute Kidney Injury: Definition, Pathophysiology and Clinical Phenotypes. Clin Biochem Rev. 2016;37(2):85–98. Gaut JP, Liapis H. Acute kidney injury pathology and pathophysiology: a retrospective review. Clin Kidney J. 2020;14(2):526–36. Hommos MS, Rule AD. Should we always defer treatment of kidney disease when there is extensive interstitial fibrosis on biopsy? Am J Nephrol. 2016;44(4):286–8. Additional Declarations No competing interests reported. Supplementary Files Supplementarytables.docx Cite Share Download PDF Status: Posted Version 1 posted 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. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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-4878222","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":338222328,"identity":"4d8b4b09-4736-40f4-928c-3edc314cdd63","order_by":0,"name":"Nisha Jose","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA/ElEQVRIiWNgGAWjYBACxgYQacCQwMDe2HAgoQLIYWZuIFILz+GDDz6cAWlhxK8FBhIYJNKSDWe2IYzBCZjb2x8+Liioy+NvyDGT5p1XG83fDtTyo2Ibbof1nDE2nmFwuFjiwBmglm3Hc2ccZmwAit7GrWVGDps0j8GBxIaDPSAtx3IbgFqYGdvwaUl//pvHoC5x/mEeoJY5x3LnE9aSYMbMY8CcuOEYG9D7DTW5GwhqAfoF6LDDiRvPMAMD+diB3I1ALQfx+cUQGGKfef7UJc67/xAYlTV1ufPOAyPoRwUeLQ2o/MNg8gBO9UAgj8avw6d4FIyCUTAKRigAAIvQYo7vfPZjAAAAAElFTkSuQmCC","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":true,"prefix":"","firstName":"Nisha","middleName":"","lastName":"Jose","suffix":""},{"id":338222331,"identity":"a32a1f6e-7261-4c79-8d72-63549a287b46","order_by":1,"name":"Sanjeet Roy","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Sanjeet","middleName":"","lastName":"Roy","suffix":""},{"id":338222333,"identity":"ec877408-67c4-4fdc-87c1-01cc1a8954ba","order_by":2,"name":"Jeethu Joseph Eapen","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Jeethu","middleName":"Joseph","lastName":"Eapen","suffix":""},{"id":338222337,"identity":"8d2d561a-9a20-4e8c-bdd9-0a2fc95c4d6b","order_by":3,"name":"Athul Thomas","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Athul","middleName":"","lastName":"Thomas","suffix":""},{"id":338222338,"identity":"eaa7ffea-9953-4c4b-8425-868a42fefbb9","order_by":4,"name":"Joseph Johnny","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Joseph","middleName":"","lastName":"Johnny","suffix":""},{"id":338222339,"identity":"2a003de9-3690-4d9a-9404-d25ed9550184","order_by":5,"name":"Selvin Sundar Raj","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Selvin","middleName":"Sundar","lastName":"Raj","suffix":""},{"id":338222340,"identity":"3f7a3b64-9708-4ac6-bd1e-e47c1d7f5667","order_by":6,"name":"Santosh Varughese","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Santosh","middleName":"","lastName":"Varughese","suffix":""},{"id":338222341,"identity":"ca06a2e3-c21c-46f2-8396-cf74c565d744","order_by":7,"name":"Suceena Alexander","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Suceena","middleName":"","lastName":"Alexander","suffix":""},{"id":338222342,"identity":"80ccdb3f-b6e2-47b0-b05c-c2d60933d6f9","order_by":8,"name":"Vinoi George David","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Vinoi","middleName":"George","lastName":"David","suffix":""},{"id":338222343,"identity":"ffdb9429-2413-4c6e-8120-53076c3d3a20","order_by":9,"name":"Reka K","email":"","orcid":"","institution":"Christian Medical College \u0026 Hospital","correspondingAuthor":false,"prefix":"","firstName":"Reka","middleName":"","lastName":"K","suffix":""}],"badges":[],"createdAt":"2024-08-08 05:23:19","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4878222/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4878222/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":66117094,"identity":"2192768c-b5b1-4511-854f-d6c80f5a86f4","added_by":"auto","created_at":"2024-10-08 00:52:54","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":22714,"visible":true,"origin":"","legend":"\u003cp\u003eConsort diagram for the study\u003c/p\u003e","description":"","filename":"Onlinedrawingimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-4878222/v1/4cc477ee63335b7bbebb9b89.png"},{"id":66117093,"identity":"87bc7289-f7e7-4b05-bc34-4a18b1d091ec","added_by":"auto","created_at":"2024-10-08 00:52:54","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":10620,"visible":true,"origin":"","legend":"\u003cp\u003eBar graph representing frequency of outcome measures in AKI\u003c/p\u003e","description":"","filename":"Onlinedrawingimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-4878222/v1/6a439e84775029c83f3abd9d.png"},{"id":66117096,"identity":"9577789d-2ecd-4044-b697-b50102c3128f","added_by":"auto","created_at":"2024-10-08 00:52:54","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":8966,"visible":true,"origin":"","legend":"\u003cp\u003eBar graph representing frequency of various biopsy findings in AKI\u003c/p\u003e","description":"","filename":"Onlinedrawingimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-4878222/v1/f755508ee0a74a453efd9617.png"},{"id":66118944,"identity":"dd228e87-7612-4271-a75e-c04178c327fb","added_by":"auto","created_at":"2024-10-08 01:08:56","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":972892,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4878222/v1/f396a4bb-b1c9-4c81-af23-18b47d7da82f.pdf"},{"id":66117095,"identity":"c26bcb58-47f6-4398-93b4-fc0a4664a495","added_by":"auto","created_at":"2024-10-08 00:52:54","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":16611,"visible":true,"origin":"","legend":"","description":"","filename":"Supplementarytables.docx","url":"https://assets-eu.researchsquare.com/files/rs-4878222/v1/29513a48e3e7b26bb0fe83f7.docx"}],"financialInterests":"No competing interests reported.","formattedTitle":" Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury ","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAKI (acute kidney injury) the term provides a convenient label to categorize a heterogenous cluster of illness all of which have differing courses and outcomes. Of the total number of renal biopsies, acute kidney injury occupies 31.7% among hospitalised patients(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). There is an increased risk, about 2–7 fold times, of bleed associated with biopsies in an acute hospitalised setting as opposed to patients undergoing routine out-patient non emergent biopsies(\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). The lack of a proper etiological diagnosis for AKI particularly when underlying causes of injury are occult, along with ambiguity on the use of drugs or toxins often forces the clinician to take on the risk of the kidney biopsy. The histopathological findings on a biopsy for acute kidney injury that actually correlate with renal recovery are unknown. This study aims to evaluate the value of the renal biopsy done for AKI in terms of its use in prognostication and renal recovery.\u003c/p\u003e \u003cp\u003eAcute kidney injury has evolved from being considered a single hit disease to being a part of a continuum that ultimately results in CKD(\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). The etiologies of AKI in the west are very different from those seen in third world countries where snake bite and diarrhoea are still of major concern. Is all AKI similar in its outcome leading to a steady progression to CKD? Is the prognosis same in a younger population with a single event of AKI and no other co-morbidities? Does a renal biopsy done in this setting really prognosticate recovery equally for all etiologies? These are some of the questions this study aims to answer.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003eA retrospective cohort study was conducted in a tertiary level hospital in South India including all patients between the time period of 2021–2023 January with a diagnosis of acute kidney injury who underwent a renal biopsy.\u003c/p\u003e\u003cp\u003eInclusion criteria:\u003c/p\u003e\u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eAdult patients with a biopsy proven diagnosis of AKI on the kidney biopsy\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e\u003cp\u003eExclusion criteria\u003c/p\u003e\u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eConcomitant glomerular disease\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eTransplant patients\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eChildren\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e\u003cp\u003eThese specific exclusion criteria of transplant and glomerular disease were chosen since in these subsets, the renal recovery may correlate with the specific glomerular pathology such as rejection or treatment of the glomerular disease rather than the AKI alone. In children outcome variables may need to be modified and the etiology of AKI is different than that seen in adults\u003c/p\u003e\u003cp\u003eData was collected from the hospital database. Certain key words were used to identify AKI on the renal biopsy reports: “acute tubular injury, acute tubular necrosis, cortical necrosis, severe tubular injury, diffuse tubular injury”. Patients who had these key words in their biopsy reports, were then screened for their eligibility into the study. Data was analysed for demography, presence and etiology of AKI as per KDIGO criteria, co-morbidities, use of dialysis and recovery parameters, death and recurrence of AKI. Specific outcome parameters were defined. The renal biopsy findings were available on the online database and these were used to correlate with specific parameters of clinical recovery. The renal biopsy data were reviewed by both a nephrologist and trained renal pathologist.\u003c/p\u003e\u003cp\u003eOutcome parameters\u003c/p\u003e\u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eThe primary outcome of the study was to evaluate the correlation between the renal biopsy report and recovery from AKI at maximum follow up.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eSecondary outcomes\u003c/p\u003e \u003cp\u003e \u003c/p\u003e\u003col style=\"list-style-type:lower-alpha;\"\u003e\n\u003cspan\u003e \u003cli\u003e \u003cp\u003eTo identify the recovery rate and follow up rate of patients with acute kidney injury\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eTo identify clincial risk factors associated with poor renal recovery and progression to CKD such as age, BMI, presence of co-morbidities, requirement and duration of KRT.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e \u003cp\u003e\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e\u003cp\u003eDefinitions used in this study\u003c/p\u003e\u003cp\u003eAKI: As defined by the KDIGO 2012 criteria(\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Refer to supplementary table 4 for criteria for baseline creatinine.\u003c/p\u003e\u003cp\u003eCo-morbidities were evaluated using the Charlston co-morbidity(\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e) and the AKI risk prediction score(\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e) was also checked for these patients.\u003c/p\u003e\u003cp\u003eRenal recovery was defined as follows\u003c/p\u003e\u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eComplete recovery: Return to baseline creatinine or normal creatinine value\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003ePartial recovery: Fall in the stage of AKI\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eNon-resolving AKI: AKI that does not resolve within 72 hours(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e)\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eResolving AKI: resolved within 72 hours\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eMAKE (Major adverse kidney events) events(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e) are defined as: either death, new requirement for dialysis or worsening of kidney function denoted by \u0026gt; 25% decline in eGFR from baseline. MAKE events were considered at 30 days, 60 days and 90 days\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eKellum classification(\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e) was also used for assessing different types of renal recovery\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e\u003cp\u003e This study was reviewed by the institutional review board of this hospital and approved. The IRB number is IRB Min no15967.\u003c/p\u003e\u003ch2\u003eStatistical analysis\u003c/h2\u003e\u003cp\u003eMean and standard deviation was reported for all the continuous variables following normality and Median and IQR (Inter Quartile Range) was reported for all the continuous variables not following normality. Frequency and percentage were reported for all the categorical variables. The parametric t-test was performed to compare the continuous variables following normality for two groups and Mann-Whitney test was performed to compare the continuous variables not following normality for two groups. Normality of the variable was assessed using rule of thumb. The Pearson Chi-square test was performed to find the association between the categorical variables. The Pie chart was plotted to show that etiology of acute kidney injury and indication for renal biopsy. The bar charts was plotted to show that frequency of outcome measures in AKI, various Kellum classes of AKI and frequency of various biopsy findings in AKI. The p-value less than 0.05 shows the statistical significance. Statistical analysis was performed using Statistical Package for Social Science (SPSS) version 21. 25.0 (IBM statistic, New York, USA).\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eThe consort diagram of the study (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e) shows that out of 420 patients identified on screening, only 54 were finally included. The majority of patients excluded were patients with concomitant glomerular disease. The patient population consisted of patients with drug or toxin induced AKI (the majority) followed by septic patients and those with snake bite AKI (Table \u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The mean age of patients was 44.9 years. Most were of normal BMI and only 61.1% of them had no known co-morbidities. About 70% of this population required dialysis and 96.3% of them had stage 3 AKI. Patient were followed by for a median of 80.50 days. Time to achieve nadir creatinine was 57 days. The mean duration of hospitalisation was 17.87 days. Among those who were on dialysis, the average time spent on dialysis was 21 days and 55.6%% became free of KRT eventually. The most commonly used modality in this study was IHD (intermittent hemodialysis) in 89.47% of patients (Table \u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). Of the total number of patients, 72.2% of patients had microhematuria and proteinuria was present in 39% of patients. Most of the renal biopsies (76%), were done for an etiological evaluation of renal dysfunction when a clear diagnosis as to the cause of AKI was not present or an alternate etiology like Acute tubule-interstitial diagnosis or rapidly progressive glomerulonephritis was entertained, while 24% were done for prognostication.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eBaseline characteristics on the study population\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCharacteristic\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFrequency\u003c/p\u003e \u003cp\u003eN\u0026thinsp;=\u0026thinsp;54\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge\u003c/p\u003e \u003cp\u003eMean (Standard Deviation)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003e44.91 (SD14.04)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eGender\u003c/b\u003e: Male : female n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e34(63%):20(37%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eAverage BMI\u003c/b\u003e\u003c/p\u003e \u003cp\u003eMean (SD)\u003c/p\u003e \u003cp\u003eMedian (IQR)\u003c/p\u003e \u003cp\u003eBMI: underweight : \u0026lt;18.5kg/m2\u003c/p\u003e \u003cp\u003eBMI normal weight: 18.5-24.9kg/m2\u003c/p\u003e \u003cp\u003eBMI Overweight: 25-29.9kg/m2\u003c/p\u003e \u003cp\u003eBMI obese\u0026thinsp;\u0026gt;\u0026thinsp;30kg/m2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e22.47 (SD45.83)\u003c/p\u003e \u003cp\u003e21.8 (19.52\u0026ndash;23.55)\u003c/p\u003e \u003cp\u003e7 (16.7)\u003c/p\u003e \u003cp\u003e26 (61.9%)\u003c/p\u003e \u003cp\u003e6 (14.3%)\u003c/p\u003e \u003cp\u003e3 (7.1%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCo-morbidities\u003c/b\u003e\u003c/p\u003e \u003cp\u003eDiabetes\u003c/p\u003e \u003cp\u003eHypertension\u003c/p\u003e \u003cp\u003ePre-existing CKD\u003c/p\u003e \u003cp\u003eChronic liver disease\u003c/p\u003e \u003cp\u003eCardiovascular disease\u003c/p\u003e \u003cp\u003eBurns or trauma\u003c/p\u003e \u003cp\u003eMajor surgery\u003c/p\u003e \u003cp\u003eOthers\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e14 (25.9%)\u003c/p\u003e \u003cp\u003e18 (33.3%)\u003c/p\u003e \u003cp\u003e6 (11.1%) (5 stage 3 and 1 stage 4)\u003c/p\u003e \u003cp\u003e3 (5.6%)\u003c/p\u003e \u003cp\u003e0\u003c/p\u003e \u003cp\u003e1 (1.9%)\u003c/p\u003e \u003cp\u003e0\u003c/p\u003e \u003cp\u003e13 (24.07%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCharlston co-morbidity score\u003c/b\u003e\u003c/p\u003e \u003cp\u003e0 score \u0026ndash; no co-morbids\u003c/p\u003e \u003cp\u003eMild (score 1,2)\u003c/p\u003e \u003cp\u003eModerate (score 3,4)\u003c/p\u003e \u003cp\u003eSevere (5 and above)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e33 (61.1)\u003c/p\u003e \u003cp\u003e13 (24.1)\u003c/p\u003e \u003cp\u003e4 (7.4)\u003c/p\u003e \u003cp\u003e4 (7.4)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCause of AKI\u003c/b\u003e\u003c/p\u003e \u003cp\u003eUrinary tract infection\u003c/p\u003e \u003cp\u003ePigment related AKI\u003c/p\u003e \u003cp\u003ePoisoning\u003c/p\u003e \u003cp\u003eDrug or toxin induced\u003c/p\u003e \u003cp\u003eSnake bite AKI\u003c/p\u003e \u003cp\u003ePancreatitis\u003c/p\u003e \u003cp\u003eSepsis\u003c/p\u003e \u003cp\u003eHypovolemia\u003c/p\u003e \u003cp\u003eHypercalcemia\u003c/p\u003e \u003cp\u003eHepato-renal syndrome\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e2\u003c/p\u003e \u003cp\u003e19\u003c/p\u003e \u003cp\u003e6\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e13\u003c/p\u003e \u003cp\u003e8\u003c/p\u003e \u003cp\u003e2\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eStage of AKI\u003c/b\u003e\u003c/p\u003e \u003cp\u003eStage 1:\u003c/p\u003e \u003cp\u003eStage 2:\u003c/p\u003e \u003cp\u003eStage 3:\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0\u003c/p\u003e \u003cp\u003e2 (3.7%)\u003c/p\u003e \u003cp\u003e52 (96.3%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eRequirement of dialysis\u003c/b\u003e\u003c/p\u003e \u003cp\u003eYes\u003c/p\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e38 (70.4%)\u003c/p\u003e \u003cp\u003e16 (29.6%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of patients on \u003cb\u003emechanical ventilation\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e8 (14.8%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of patients on \u003cb\u003einotropes\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5 (9.3%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eAKI risk prediction score\u003c/b\u003e\u003c/p\u003e \u003cp\u003eLow (0-2.9)\u003c/p\u003e \u003cp\u003eModerate (3-8.9)\u003c/p\u003e \u003cp\u003eHigh (9-11.5)\u003c/p\u003e \u003cp\u003eVery high (more than 11.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e22 (40.7)\u003c/p\u003e \u003cp\u003e30 (55.6)\u003c/p\u003e \u003cp\u003e2 (3.7)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eSite of admission\u003c/b\u003e\u003c/p\u003e \u003cp\u003eOutpatient\u003c/p\u003e \u003cp\u003eWard\u003c/p\u003e \u003cp\u003eICU\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0\u003c/p\u003e \u003cp\u003e37 (68.5%)\u003c/p\u003e \u003cp\u003e17 (31.5%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eDuration of hospitalization\u003c/b\u003e\u003c/p\u003e \u003cp\u003eMean (SD)\u003c/p\u003e \u003cp\u003eMedian (IQR)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e17.87 (SD45.22)\u003c/p\u003e \u003cp\u003e10 (5.75\u0026ndash;17.25)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMean \u003cb\u003eAdmission creatinine\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6.65 (5.13)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eDays to reach maximum creatinine value\u003c/b\u003e\u003c/p\u003e \u003cp\u003eMean (SD)\u003c/p\u003e \u003cp\u003eMedian (IQR)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e134.72 (SD188.57)\u003c/p\u003e \u003cp\u003e4 (\u003cspan additionalcitationids=\"CR2 CR3 CR4 CR5 CR6 CR7 CR8 CR9 CR10 CR11 CR12 CR13\" citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eNadir creatinine\u003c/b\u003e\u003c/p\u003e \u003cp\u003eMean (SD)\u003c/p\u003e \u003cp\u003eMedian (IQR)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2.61 (SD2.52)\u003c/p\u003e \u003cp\u003e1.51 (0.93\u0026ndash;3.86)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eDays to reach nadir value of creatinine\u003c/b\u003e\u003c/p\u003e \u003cp\u003e\u003cb\u003eMean (SD)\u003c/b\u003e\u003c/p\u003e \u003cp\u003e\u003cb\u003eMedian\u003c/b\u003e (IQR)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e134.72 (SD188.57)\u003c/p\u003e \u003cp\u003e57 (15.75\u0026ndash;177.50)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eDuration of follow up\u003c/b\u003e\u003c/p\u003e \u003cp\u003eMean (SD)\u003c/p\u003e \u003cp\u003eMedian (IQR)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e186.68 (SD249.19)\u003c/p\u003e \u003cp\u003e80.50 (24.50-229.25)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCreatinine at maximum follow up\u003c/b\u003e\u003c/p\u003e \u003cp\u003e\u003cb\u003eMean (SD)\u003c/b\u003e\u003c/p\u003e \u003cp\u003e\u003cb\u003eMedian\u003c/b\u003e (IQR)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3.67 (SD4.49)\u003c/p\u003e \u003cp\u003e1.69 (0.94\u0026ndash;5.24)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eDetails of the use of dialysis for AKI\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCharacteristic\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFrequency (percentage)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of \u003cb\u003epatients on KRT\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e38 (70.4%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eType of KRT used (n\u0026thinsp;=\u0026thinsp;38)\u003c/b\u003e\u003c/p\u003e \u003cp\u003eIHD\u003c/p\u003e \u003cp\u003eSLED\u003c/p\u003e \u003cp\u003eCRRT\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e(Some patients used multiple modalities)\u003c/p\u003e \u003cp\u003e34 (89.47%)\u003c/p\u003e \u003cp\u003e5 (13.16%)\u003c/p\u003e \u003cp\u003e1 (2.63%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of sessions\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.45\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eNumber of days on KRT\u003c/b\u003e\u003c/p\u003e \u003cp\u003eMean (SD)\u003c/p\u003e \u003cp\u003eMedian\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e22.48 (SD4.83)\u003c/p\u003e \u003cp\u003e21.8 (0\u0026ndash;18.00)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of patients who became \u003cb\u003efree of KRT\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e30 (55.6%)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eWhen looking at various outcome measures of AKI, the incidence of MAKE events at 30 days was found to be 7.4% which decreased to 3.7% at 60 and 90 days (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). All patients in this cohort had persistent AKI (i.e., persisting beyond 48 hours). Partial recovery was seen in 33.3% and complete recovery in 38.9%. Overall, 72.2% of patients showed some form of renal recovery. Only 1 patient died in this cohort. Most patients (98.1%) had AKD (acute kidney disease) and 44.4% of them were labelled as CKD (chronic kidney disease) subsequently. Most patients were classified as Kellum class 4 i.e., without complete recovery at hospital discharge but showing some form of renal recovery. Among the clinical features, the cause of AKI, presence of pre-existing CKD and Charleston co-morbidity score seemed to correlate negatively with independence from KRT (Table \u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). Among the laboratory parameters the admission creatinine and maximum creatinine and days taken to reach the nadir correlated negatively with independence from KRT and complete recovery of the renal injury. Presence or absence of AKD did not seem to have any bearing on long term renal recovery of independence from KRT.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTable representing correlation of various clinical characteristics with outcome measures of AKI\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"6\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eP value for partial recovery\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eComplete recovery\u003c/p\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eIndependence from KRT\u003c/p\u003e \u003cp\u003eP Value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eTransitioned to CKD\u003c/p\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eComposite of renal recovery and independence from KRT\u003c/p\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.201\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.637\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.829\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.715\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.874\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGender\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.84\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.480\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.950\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.553\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.328\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBMI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.432\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.524\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.373\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.324\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.769\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eStage of AKI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.54\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.147\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.193\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCause of AKI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.39\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.12\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.38\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.006\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.86\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRequirement of KRT\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.14\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.089\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.235\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.734\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCo-morbidities\u003c/b\u003e\u003c/p\u003e \u003cp\u003eDiabetes\u003c/p\u003e \u003cp\u003eHypertension\u003c/p\u003e \u003cp\u003ePre-existing CKD\u003c/p\u003e \u003cp\u003eStage of CKD\u003c/p\u003e \u003cp\u003eCLD\u003c/p\u003e \u003cp\u003eBurns or trauma\u003c/p\u003e \u003cp\u003eMajor surgery\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.18\u003c/p\u003e \u003cp\u003e0.54\u003c/p\u003e \u003cp\u003e0.65\u003c/p\u003e \u003cp\u003e0.767\u003c/p\u003e \u003cp\u003e0.25\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e0.418\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.77\u003c/p\u003e \u003cp\u003e0.55\u003c/p\u003e \u003cp\u003e0.386\u003c/p\u003e \u003cp\u003e0.778\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e0.389\u003c/p\u003e \u003cp\u003e0.017\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.890\u003c/p\u003e \u003cp\u003e0.245\u003c/p\u003e \u003cp\u003e0.005\u003c/p\u003e \u003cp\u003e0.005\u003c/p\u003e \u003cp\u003e0.575\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e0.720\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.115\u003c/p\u003e \u003cp\u003e0.051\u003c/p\u003e \u003cp\u003e0.027\u003c/p\u003e \u003cp\u003e0.056\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e0.42\u003c/p\u003e \u003cp\u003e0.012\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.407\u003c/p\u003e \u003cp\u003e0.487\u003c/p\u003e \u003cp\u003e0.018\u003c/p\u003e \u003cp\u003e0.018\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e1\u003c/p\u003e \u003cp\u003e0.356\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCharlston co-morbidity score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.08\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.507\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.005\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.038\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.537\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMechanical ventilation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.70\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.277\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInotropes requirement\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.144\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.442\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.306\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAKI risk prediction score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.628\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.238\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.273\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.341\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAdmission creatinine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.811\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.579\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.009\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.826\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.441\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eMaximum creatinine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.970\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.785\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.411\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.983\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDays to reach maximum creatinine value\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.800\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.175\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.841\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.180\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.820\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003enadir value of creatinine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.130\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.251\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.002\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDays to reach nadir value of creatinine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.419\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.028\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.009\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.653\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eType of KRT used\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.44\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.078\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.126\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.227\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of sessions\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.428\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.046\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.067\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.880\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNumber of days on KRT\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.483\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.039\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.062\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.970\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFree of KRT\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.004\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.851\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e----\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.609\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e-----\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKellum class\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.102\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.002\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAKD\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.389\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.444\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.442\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eThe frequency of various biopsy findings in acute kidney injury is presented in Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e. 92.6% of patients had diffuse involvement of tubules on renal biopsy. Cortical involvement in the form of cortical necrosis was seen in 5.6% of patients. The most frequent finding on the renal biopsy was dilatation of tubules followed by flattening of the tubular lining epithelium. 77.8% of cases the brush border was damaged. Chronic vascular sclerotic changes were present in 61.1% of patients. Interstitial fibrosis and tubular atrophy (IFTA) was present in 50% of patients. The association of diabetes with glomerulosclerosis on the kidney biopsy in this setting was not significant (p value 0.568) however, hypertension was significantly associated with glomerulosclerosis (p value of 0.203). The presence of IFTA was significantly correlated with diabetes (p value 0.295) but not associated with presence of hypertension (p value of 0.614). Vascular changes were not significantly associated with diabetes or hypertension in this setting (p value 0.758 and 0.713 respectively). Pre-exiting CKD was significantly correlated with both presence of glomerulosclerosis, IFTA and atherosclerosis. Severe degrees of glomerular injury are generally absent in cases of acute kidney injury. The only biopsy finding which correlated with independence from KRT was presence of sloughing (Table \u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e4\u003c/span\u003e). Recovery both complete and partial, had a correlation with presence of chronic vascular sclerotic changes. IFTA correlated with progression to chronic kidney disease. Presence of vacuolization on the renal biopsy correlated with complete recovery.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab4\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eCorrelation of biopsy findings with various outcome measures in AKI\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"6\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eP value for partial recovery\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eComplete recovery\u003c/p\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eIndependence from KRT p value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eTransitioned to CKD p value\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eComposite of renal recovery and independence from KRT\u003c/p\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSite of involvement\u003c/p\u003e \u003cp\u003eCortex or\u003c/p\u003e \u003cp\u003eMedulla\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.543\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.274\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.579\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.243\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.121\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"6\" nameend=\"c6\" namest=\"c1\"\u003e \u003cp\u003e\u003cb\u003eTubular changes due to AKI\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDegree of involvement\u003c/p\u003e \u003cp\u003eFocal or Diffuse-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.638\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of sloughing\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.97\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.016\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.728\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.708\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of flattening\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1.00\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.618\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of dilation of tubules\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.287\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.564\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of necrosis of tubules\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.30\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.117\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.359\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.152\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.485\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRegenerative changes noted on biopsy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.253\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.415\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.373\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.071\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresence of Vacuolization of tubules\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.512\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.028\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.890\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.708\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.261\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLoss of brush border\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.747\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.272\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.470\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.714\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDenudation of the tubular basement membrane\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.389\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.442\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTubular cell calcification\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.723\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.165\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.680\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"6\" nameend=\"c6\" namest=\"c1\"\u003e \u003cp\u003e\u003cb\u003eInterstitial changes due to AKI\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInterstitial edema\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.846\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.272\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.667\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.388\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.556\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIFTA more than 25%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.634\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.066\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.565\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.008\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"6\" nameend=\"c6\" namest=\"c1\"\u003e \u003cp\u003e\u003cb\u003eGlomerular changes due to AKI\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlomerulosclerosis more than 25%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.549\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.518\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.677\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.320\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.179\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"6\" nameend=\"c6\" namest=\"c1\"\u003e \u003cp\u003e\u003cb\u003eVascular changes identified\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eArteriosclerosis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.016\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.003\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.534\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.027\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e0.495\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe exact prognostic value of a kidney biopsy in the setting of AKI has not been studied previously. This study looks at both clinical and renal biopsy prognostic variables in renal recovery from AKI in the setting of a developing country where the etiology and setting of AKI is often different from that seen in the developed world.\u003c/p\u003e \u003cp\u003eThe patient population\u003c/p\u003e \u003cp\u003eThe transplant and glomerulonephritis cohorts have been included in other research on AKI(\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). However, when looking at the pathology of AKI it was essential to exclude these patients since glomerulonephritis cause specific pathological changes in the kidney which might confound the interpretation of the extent of involvement of the acute kidney injury on the renal biopsy. The most common cause of AKI in this cohort was drug or toxin induced acute kidney injury and septic AKI (Table \u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). In data from the Indian society of nephrology AKI registry, sepsis (34.7%) and tropical fevers (9.8%) were considered to be the most common etiology of community acquired AKI followed by AKI associated with liver disease (9.1%) (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e). Snake bite AKI is also fairly common in these regions. The difference is the etiological diagnosis in this study when compared to others on AKI is likely because only patients who underwent a kidney biopsy were included. The co-morbidity profile (Table \u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e) is similar to that observed in the ISN registry with hypertension being the most common co-morbidity and diabetes following closely. When compared to data from developed nations, it is noted that AKI in the developing world occurs more frequently in younger patients with fewer co-morbidities as opposed to the developed world where older populations with more number of comorbidities develop AKI(\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). The cohort in this research study were individuals who had severe AKI, that is most of them required dialysis and more than 95% of them had stage 3 AKI. This data is in keeping with prospective studies done in India where more than 50% of patients have AKI stage 3(\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eFollow up and outcome measures\u003c/p\u003e \u003cp\u003ePatients were followed up for a median of 80.50 days (Table \u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Data from other studies showed that only about 13-37.3%(\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e) of patients with AKI remain on follow up with a nephrologist among Medicare patients(\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). Follow up needs to be streamlined for better patient outcomes especially in high-risk patients.\u003c/p\u003e \u003cp\u003eTraditionally it is considered that recovery from AKI follows 4 steps, initiation, maintenance, polyuria and restitution. Renal recovery is expected to occur within 3 month, if it doesn\u0026rsquo;t if is labelled CKD(\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). In this study however, although most patients who stop dialysis do so over a mean of 22.48 days, recovery takes much longer with nadir creatinine generally being achieved over a period of 57 days or more. This is in keeping with data from the mayo clinic services, most patients were able to discontinue dialysis before 6 months while the remaining recovered over a period of 12 months. This may be an important take home message from this data, that recovery occurs slowly and can be anticipated even after 3 months.\u003c/p\u003e \u003cp\u003eA majority (55.6%) of patients on dialysis became free of dialysis during the course of their treatment (Table \u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). When compared to western data, this number is low in that among 50% of AKD patients who have survived their initial hospitalisation, only 30% generally required continuation of KRT(\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). The higher number in this cohort maybe due to the selection bias of patients. Patients who are likely to not recover AKI, were more likely to require kidney biopsies for prognostication or to provide an alternate diagnosis for the kidney injury.\u003c/p\u003e \u003cp\u003eThe clinical characteristic that correlated with renal recovery and outcome measures such as independence from KRT (Table \u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e) is similar to those documented in another study where underlying CKD and presence of co-morbidities corelate poorly for these measures(\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). It is interesting to note that labelling the disease as AKD does not portend a poor prognosis for renal recovery. Another interesting finding is that not just the nadir creatinine that correlates with composite measures of renal recovery but also the time to achieve the nadir. This may give us an early clue likelihood of renal recovery even before nadir creatinine is achieved.\u003c/p\u003e \u003cp\u003eThe urine sediment\u003c/p\u003e \u003cp\u003ePre-renal AKI is known to have a bland sediment, while in ATN urine may show hematuria and muddy brown casts. Automated analysers are less sensitive and specific to detect these casts when compared with a nephrologist interpretation of the urine sediment(\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e). In this cohort, automated analysers were used to assess urine and the difficulty is often differentiating a severe AKI which has caused ATN from a glomerular disease. This may be a contributing factor to the number of biopsies that were done in the acute phase of the illness to rule out a glomerular disorder.\u003c/p\u003e \u003cp\u003eOutcome measures of AKI\u003c/p\u003e \u003cp\u003eWhen it comes to measuring renal recovery, there is no dearth of outcome measures(\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e). The myriad different interpretations of renal recovery and measures make comparing data between studies difficult. Some examples of renal recovery measures that are used in various studies are MAKE DC, 30, 60,90 and 1 year events, while others look at partial recovery (defined variably in different studies) vs. complete recovery. Still other studies look at AKI as transient or persistent based on a 48-hour window. To make the results comparable, we looked at all these outcome variables in AKI, MAKE 30 events were very low, as were MAKE 60, and 90 events (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). In data from another trial the incidence of MAKE is approximately 30%(\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e). These may represent a selection bias in that only patients who survived this initial episode of AKI and were fit for biopsy were included in this study. However, it should be remembered that, most of this cohort were dialysis requiring AKI and the number of MAKE events is much lower than expected. One possible reason is the etiology of AKI which is different than the west and the lower co-morbidity burden of this population. Kellum et al suggested a novel method of quantifying recovery based on timing and degree of recovery. This classification showed the pattern of renal recovery and in other data proved to predict long term outcomes(\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). In this cohort the Kellum classes had good correlation with other measures of renal recovery such as complete recovery and independence from KRT (Table \u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eBiopsy findings in AKI\u003c/p\u003e \u003cp\u003eThe relative frequency of biopsy findings is shown in Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e. In a systematic review of biopsy findings in AKI, A similar pattern to this one was noted by Wen et al(\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). As in this study, tubular sloughing was a common finding followed by epithelial cell flattening and simplification. Very little data is available worldwide correlating biopsy findings with clinically significant outcomes for AKI. One such study was a post-mortem analysis of patients who underwent kidney biopsy for acute kidney injury in COVID-19 patients(\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e). The only histopathological finding that correlated with severity of AKI and recovery was presence of pigmented casts.\u003c/p\u003e \u003cp\u003eThis study provides new insight and findings into correlation of biopsy findings with renal recovery and independence from KRT. As can be expected, chronic vascular sclerotic changes on the renal biopsy have significant correlation with renal recovery (Table \u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e4\u003c/span\u003e). This is possibly because the pathophysiology of acute kidney injury is closely linked to renal vasoconstriction, endothelial injury and activation of inflammatory pathways(\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). It makes sense that poor blood supply with arteriosclerotic vessels would play an important role in renal recovery. Vacuolisation is commonly seen in drug and toxin induced AKI due to ART (anti-retroviral therapy), CNI (calcineurin inhibitors) and contrast media and hence probably has a specific correlation with etiology and renal recovery(\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e). Interstitial fibrosis and tubular atrophy in several glomerular diseases has been liked to disease progression(\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThis study is a first-of-its-kind cohort study looking at renal biopsy findings and correlating them with renal recovery however, the selection bias of the study, to include only biopsy proven AKI, will limit the generalisability of the data to all AKI.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eRenal recovery occurs slowly with nadir creatinine being achieved over a mean of 57 days. Clinical characteristics associated negatively with independence from KRT include presence of pre-existing CKD and the Charleston comorbidity index. Renal biopsy findings that corelate positively with progression to CKD include presence of interstitial fibrosis and tubular atrophy. Chronic vascular sclerotic changes on a renal biopsy have significant negative correlation with renal recovery. The degree of glomerular damage does not correlate with recovery from AKI.\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eDisclosure:\u003c/h2\u003e \u003cp\u003eDr Jose et al have no conflicts of interest to disclose\u003c/p\u003e \u003ch2\u003eFunding:\u003c/h2\u003e \u003cp\u003eNo external funding was used for this study\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eNJ, SR, RK, JJ and SSR wrote the main manuscript and prepared figuresATJ, JJE, SV, SA, VGD reviewed and edited the manuscript\u003c/p\u003e\u003ch2\u003eAcknowledgement\u003c/h2\u003e\u003cp\u003eI acknowledge Mr Srinivasan statistician working in christian medical college for his help with the statisitics\u003c/p\u003e\u003ch2\u003eData sharing:\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eall the data that support the findings is included in the manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eAbuduwupuer Z, Lei Q, Liang S, Xu F, Liang D, Yang X, et al. The Spectrum of Biopsy-Proven Kidney Diseases, Causes, and Renal Outcomes in Acute Kidney Injury Patients. Nephron. 2023;147(9):541\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWaikar SS, McMahon GM. Expanding the Role for Kidney Biopsies in Acute Kidney Injury. Semin Nephrol. 2018;38(1):12\u0026ndash;20.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTakaori K, Yanagita M. Insights into the Mechanisms of the Acute Kidney Injury-to-Chronic Kidney Disease Continuum. Nephron. 2016;134(3):172\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKhwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract. 2012;120(4):c179\u0026ndash;184.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCharlson ME, Carrozzino D, Guidi J, Patierno C. Charlson Comorbidity Index: A Critical Review of Clinimetric Properties. Psychother Psychosom. 2022;91(1):8\u0026ndash;35.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMalhotra R, Kashani KB, Macedo E, Kim J, Bouchard J, Wynn S, et al. A risk prediction score for acute kidney injury in the intensive care unit. Nephrol Dial Transpl. 2017;32(5):814\u0026ndash;22.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAssociation Between Early Recovery of Kidney Function After Acute Kidney Injury and Long-. term Clinical Outcomes | Nephrology | JAMA Network Open | JAMA Network [Internet]. [cited 2024 Mar 16]. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://jamanetwork.com/journals/jamanetworkopen/fullarticle/2764347\u003c/span\u003e\u003cspan address=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2764347\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBillings FT, Shaw AD. Clinical trial endpoints in acute kidney injury. Nephron Clin Pract. 2014;127(1\u0026ndash;4):89\u0026ndash;93.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKellum JA, Sileanu FE, Bihorac A, Hoste EAJ, Chawla LS. Recovery after Acute Kidney Injury. Am J Respir Crit Care Med. 2017;195(6):784\u0026ndash;91.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAbuduwupuer Z, Lei Q, Liang S, Xu F, Liang D, Yang X, et al. The Spectrum of Biopsy-Proven Kidney Diseases, Causes, and Renal Outcomes in Acute Kidney Injury Patients. Nephron. 2023;147(9):541\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePrasad N, Jaiswal A, Meyyappan J, Gopalakrishnan N, Chaudhary AR, Fernando E et al. Community-acquired acute kidney injury in India: data from ISN-acute kidney injury registry. Lancet Reg Health - Southeast Asia [Internet]. 2024 Feb 1 [cited 2024 Feb 21];21. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.thelancet.com/journals/lansea/article/PIIS2772-3682(24)00009-X/fulltext\u003c/span\u003e\u003cspan address=\"https://www.thelancet.com/journals/lansea/article/PIIS2772-3682(24)00009-X/fulltext\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYang L. Acute Kidney Injury in Asia. Kidney Dis. 2016;2(3):95\u0026ndash;102.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePriyamvada PS, Jayasurya R, Shankar V, Parameswaran S. Epidemiology and Outcomes of Acute Kidney Injury in Critically Ill: Experience from a Tertiary Care Center. Indian J Nephrol. 2018;28(6):413\u0026ndash;20.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWu VC, Chueh JS, Chen L, Huang TM, Lai TS, Wang CY, et al. Nephrologist Follow-Up Care of Patients With Acute Kidney Disease Improves Outcomes: Taiwan Experience. Value Health. 2020;23(9):1225\u0026ndash;34.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSilver SA, Siew ED. Follow-up Care in Acute Kidney Injury: Lost in Transition. Adv Chronic Kidney Dis. 2017;24(4):246\u0026ndash;52.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePatschan D, M\u0026uuml;ller GA. Acute kidney injury. J Inj Violence Res. 2015;7(1):19\u0026ndash;26.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eClark EG, James MT, Hiremath S, Sood MM, Wald R, Garg AX, et al. Predictive Models for Kidney Recovery and Death in Patients Continuing Dialysis as Outpatients after Starting in Hospital. Clin J Am Soc Nephrol. 2023;18(7):892.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGodin M, Macedo E, Mehta RL. Clinical Determinants of Renal Recovery. Nephron Clin Pract. 2014;127(1\u0026ndash;4):25\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCavanaugh C, Perazella MA. Urine Sediment Examination in the Diagnosis and Management of Kidney Disease: Core Curriculum 2019. Am J Kidney Dis. 2019;73(2):258\u0026ndash;72.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKellum JA. How Can We Define Recovery after Acute Kidney Injury? Considerations from Epidemiology and Clinical Trial Design. Nephron Clin Pract. 2014;127(1\u0026ndash;4):81\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSparks M, Renal Fellow N. 2022 [cited 2024 Feb 28]. Making Sense of Make (Major Adverse Kidney Events) After AKI. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.renalfellow.org/2022/10/05/making-sense-of-make-major-adverse-kidney-events-after-aki/\u003c/span\u003e\u003cspan address=\"https://www.renalfellow.org/2022/10/05/making-sense-of-make-major-adverse-kidney-events-after-aki/\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGameiro J, Marques F, Lopes JA. Long-term consequences of acute kidney injury: a narrative review. Clin Kidney J. 2021;14(3):789\u0026ndash;804.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWen Y, Yang C, Menez SP, Rosenberg AZ, Parikh CR. A Systematic Review of Clinical Characteristics and Histologic Descriptions of Acute Tubular Injury. Kidney Int Rep. 2020;5(11):1993\u0026ndash;2001.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRivero J, Merino-L\u0026oacute;pez M, Olmedo R, Garrido-Roldan R, Moguel B, Rojas G, et al. Association between Postmortem Kidney Biopsy Findings and Acute Kidney Injury from Patients with SARS-CoV-2 (COVID-19). Clin J Am Soc Nephrol CJASN. 2021;16(5):685\u0026ndash;93.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMakris K, Spanou L. Acute Kidney Injury: Definition, Pathophysiology and Clinical Phenotypes. Clin Biochem Rev. 2016;37(2):85\u0026ndash;98.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGaut JP, Liapis H. Acute kidney injury pathology and pathophysiology: a retrospective review. Clin Kidney J. 2020;14(2):526\u0026ndash;36.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHommos MS, Rule AD. Should we always defer treatment of kidney disease when there is extensive interstitial fibrosis on biopsy? Am J Nephrol. 2016;44(4):286\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"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":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"","lastPublishedDoi":"10.21203/rs.3.rs-4878222/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4878222/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eIntroduction: Acute kidney injury (AKI) is no longer considered a single hit disease but part of a spectrum that culminates in adverse renal and cardiovascular outcomes. What are the renal biopsy findings of patient with persistent AKI/AKD (acute kidney disease)? Are there renal biopsy characteristics which predict renal recovery. These are the questions that this study addresses.\u003c/p\u003e \u003cp\u003eMethodology: A retrospective study was conducted analyzing all patients who underwent a renal biopsy with a diagnosis of acute kidney injury from January 2021 to January 2023 from the online hospital database. Patients with other glomerular disease and transplant patients were excluded from this cohort. The clinical and renal biopsy characteristics were analyzed for their correlation with renal recovery.\u003c/p\u003e \u003cp\u003eResults: Of 420 patients screened, 54 were included in the study. Most patients had stage 3 AKI. The median follow up in this study was 80.50 days. Among those on dialysis, 55.6% of patients became free of KRT (kidney replacement therapy). 92.6% of the study population had diffuse tubular involvement on the renal biopsy. Clinical recovery correlated with the degree of vasculature involvement on the renal biopsy. Interstitial fibrosis and tubular atrophy corelated with progression to CKD. Among the clinical features, the cause of AKI, presence of pre-existing CKD and Charleston co-morbidity score correlated with independence from KRT.\u003c/p\u003e \u003cp\u003eConclusion: Specific findings on the renal biopsy such as atherosclerotic changes correlate negatively with long-term recovery in AKI and renal biopsy findings of interstitial fibrosis and tubular atrophy may help to prognosticate progression to CKD.. Among clinical characteristics, the presence of co-morbidities and pre-existing CKD correlates negatively with renal recovery.\u003c/p\u003e","manuscriptTitle":" Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury ","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-10-08 00:52:49","doi":"10.21203/rs.3.rs-4878222/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"
[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"7f4fb737-f490-4fa7-a55d-f7775b3c8bb9","owner":[],"postedDate":"October 8th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2024-10-08T00:52:52+00:00","versionOfRecord":[],"versionCreatedAt":"2024-10-08 00:52:49","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4878222","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4878222","identity":"rs-4878222","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}
Text is read by the "Ask this paper" AI Q&A widget below.
Extraction quality varies by source — PMC NXML preserves structure
cleanly, OA-HTML may include some navigation residue, and OA-PDF can
have broken hyphenation. The publisher copy
(via DOI)
is the canonical version.