Retrospective Analysis of Glucocorticoid Therapy in Pediatric immunoglobulin A Nephropathy: Kidney Outcomes and Efficacy

Retrospective Analysis of Glucocorticoid Therapy in Pediatric immunoglobulin A Nephropathy: Kidney Outcomes and Efficacy | 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 Retrospective Analysis of Glucocorticoid Therapy in Pediatric immunoglobulin A Nephropathy: Kidney Outcomes and Efficacy Heyan Wu, Zhengkun Xia, Lidan Zhang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5996564/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 15 Jul, 2025 Read the published version in Pediatric Nephrology → Version 1 posted 5 You are reading this latest preprint version Abstract Background : The efficacy of glucocorticoid (GC) in the management of immunoglobulin A nephropathy (IgAN) remains highly controversial. The study was conducted to analyze the efficacy and kidney outcomes of GC in the treatment of pediatric IgAN. Methods: Using the follow-up data of children with chronic kidney disease from the Department of Pediatrics at Jinling Hospital between January 2000 and December 2020, we selected children with primary IgAN who were ≤18 years old, confirmed by renal biopsy, and had undergone regular follow-up for more than 2 years. Patients who had previously used other immunosuppressive agents or had not received renin-angiotensin system blocker (RASB) treatment were excluded. The selected patients were divided into two groups based on their prior treatment regimens: the GC+RASB group and the RASB group. The primary outcome was a composite of a 40% decrease in estimated glomerular filtration rate (eGFR) from baseline, kidney failure, or death due to kidney disease. Results: A total of 374 patients (149 females) were enrolled, with 230 in the GC+RASB group and 144 in the RASB group. At baseline, the GC+RASB group had lower albumin and higher creatinine levels (all P < 0.05). From 6 months of treatment, the GC+RASB group showed higher urinary protein remission rates ( P < 0.05), but hematuria relief was similar between groups. Adverse events, including centripetal obesity, were more frequent in the GC+RASB group ( P = 0.001). After a median follow-up of 130.97 months, the GC+RASB group had fewer endpoint events (5.22% vs. 11.11%, P = 0.035) and higher cumulative kidney survival rates, particularly in patients with eGFR >50 ml/min/1.73m² and 24h-UP ≥1 g/d (all P 50 ml/min/1.73 m² and proteinuria ≥1 g/d. No additional kidney survival benefit was observed in children with eGFR ≤50 ml/min/1.73 m² or proteinuria <1 g/d. IgA nephropathy Glucocorticoids Renin-angiotensin system blocker Children Kidney Outcomes Figures Figure 1 Introduction Immunoglobulin A nephropathy (IgAN) is a major cause of chronic glomerulonephritis in East Asia and represents a global health issue affecting both pediatric and adult populations. In adults, 1–2% progress to end-stage kidney disease (ESKD) annually, and approximately 50% reach kidney failure within 20–30 years[ 1 ]. The prognosis for childhood IgAN is as severe as in adults, with 10–13% of pediatric patients progressing to ESKD within 10 years of follow-up and 20–30% doing so within 20 years [ 2 , 3 ]. The pathogenesis of IgAN is characterized by immune dysregulation mediated by aberrantly glycosylated IgA1 in the hinge region[ 4 ]. Renin-angiotensin system blockers (RASB) have established renoprotective effects in both adult and pediatric IgAN and are considered first-line therapy. Multiple studies in adults, like the APPROACH study[ 5 ], have demonstrated the efficacy of RASB in reducing proteinuria and potentially delaying disease progression. In children, although data are more limited, studies support the use of RASB based on the similar underlying pathophysiological mechanisms related to renin-angiotensin system activation in IgAN[ 6 , 7 ]. However, glucocorticoid (GC) efficacy remains controversial[ 8 ]. According to the KDIGO guidelines[ 9 ], GC should be restricted to IgAN patients with persistent proteinuria and preserved renal function, while other immunosuppressants are generally discouraged. GC therapy has shown efficacy in reducing proteinuria and slowing renal function decline in IgAN, as evidenced by multiple clinical trials[ 10 – 12 ]had demonstrated that GC treatment can diminish proteinuria and postpone kidney function deterioration in IgAN. On the other hand, trials like the STOP - IgAN trial[ 13 ], which showed that immunosuppressive treatment including GC can reduce proteinuria yet there was no difference in 3 - year renal function endpoints, had raised concerns about the long -term benefits. The TESTING study[ 14 ] showed that a reduced-dose glucocorticoid regimen had similar effects on reducing proteinuria and protecting renal function as a full-dose regimen but with significantly fewer adverse effects. In the pediatric population, the situation is more complex. The use of GC in pediatric IgAN is based on the assumption that the underlying immune - mediated pathogenesis is similar to adults. However, due to the potential impact of GC on growth and development in children, the decision - making process is more challenging. The Validation Study of the Oxford Classification of IgA nephropathy (VALIGA) [ 15 ]showed that children < 16 years treated with GC had a significantly reduced risk of progression towards ESKD. But the overall evidence base is still not as robust as in adults, and long-term follow-up studies are needed to assess potential impacts on growth and the developing immune system. Given these considerations, further research is needed to explore the impact of GCs on the prognosis of children with IgAN. Understanding the balance between the benefits and risks of GC therapy in this population is crucial for optimizing individualized treatment strategies. This study aims to improve the understanding of pediatric IgAN and provide a theoretical foundation for more effective and safer clinical management. Methods Study design and participants This retrospective cohort study evaluated pediatric patients (≤ 18 years) with biopsy-proven IgAN treated at Jinling Hospital between January 2000 and December 2020.Eligible participants were stratified into two treatment groups based on the use of glucocorticoids: the RASB monotherapy group (RASB group) and the GC combined with RASB therapy group (GC + RASB group). We excluded patients with any of the following: (1) secondary IgA nephropathy (e.g., due to chronic liver disease, rheumatoid arthritis, Henoch-Schönlein purpura, or ankylosing spondylitis);(2) indications for intensive glucocorticoid therapy (e.g., crescentic IgAN); (3) contraindications to GC(e.g., severe infections, active tuberculosis, malignancy, or uncontrolled hypertension);(4) use of other immunosuppressive agents within 1 year before or after treatment; (5) acute kidney injury or other causes of unstable renal function. All participants were followed for at least two years, with final follow-up data collected through September 30, 2024. Our study was a retrospective analysis, and the selected patients were divided into two groups based on their prior treatment regimens. In clinical practice, the decision to use GC + RASB or RASB alone was primarily based on a combination of clinical judgment and biopsy results. Specifically, patients with more severe histological changes (such as higher degrees of glomerulosclerosis or more pronounced interstitial fibrosis) and higher levels of proteinuria were more likely to be treated with GC + RASB. Conversely, patients with milder pathological changes and lower levels of proteinuria were more often treated with RASB alone. Oral GC was initiated at 1 mg/kg/day (max 60 mg/day) for 4–6 weeks, then tapered by 5 mg every 2 weeks until reaching 0.5 mg/kg/day, followed by a reduction of 2.5-5 mg every 2–4 weeks until discontinuation, with a total treatment duration of 6 months. Data collection The study utilized retrospective medical record data from this patient cohort, with all follow-up information current through September 2024. Collected clinical parameters encompassed demographic characteristics (sex and age at diagnosis) and therapeutic interventions. Hemodynamic assessment incorporated mean arterial pressure (MAP), Systolic blood pressure (SBP) and Diastolic blood pressure (DBP). Longitudinal monitoring included treatment response evaluation, renal outcomes, and immunosuppressive regimen details. Biological specimens (blood and urine) were obtained concurrently with renal biopsy procedures. Serum markers: Albumin (Alb), lipid profile (cholesterol and triglycerides), uric acid(UA), serum immunoglobulin levels (IgG, IgA, IgM), complement 3 (C3), and renal function parameters [estimated glomerular filtration rate(eGFR) and serum creatinine (Scr)]. Urinary biomarkers:24-hour urinary protein(24h-UP), urinary α-2-macroglobulin(uα2-m), urinary N-acetyl-β-D-glucosaminidase (uNAG), urinary retinol-binding protein(uRBP), and urine complement3(uC3). Outcomes The primary composite endpoint consisted of a ≥ 40% decline in eGFR from the baseline, progression to kidney failure (which was defined as the need for maintenance dialysis or kidney transplantation), or death caused by kidney disease, and this is consistent with that in The TESTING Randomized Clinical Trial[ 16 ]. The safety endpoint recorded adverse events related to GC, including episodes of infection, hepatic dysfunction, central obesity, and hyperglycemia. Definitions The eGFR was calculated using the Schwartz formula[ 17 ] or CKD-EPI equation[ 18 ] (> 16 years)],. We quantified the rate of eGFR decline during the follow-up period. Complete proteinuria remission was defined as a 24-hour urine protein excretion < 200 mg/day for pediatric patients, consistent with the KDIGO Clinical Practice Guidelines for Glomerular Diseases[ 19 ]. Children were considered to have hypertension if their systolic or diastolic blood pressure continuously exceeds the 95th percentile of children of the same age, gender, and height[ 20 ].Mean arterial pressure (MAP), derived using the standard formula: [(SBP + 2 × DBP)/3]. Renal biopsy specimens were graded based on the Oxford Classification[ 21 ]. Crescentic IgAN was defined as IgAN with more than 50% of glomeruli showing crescents[ 22 ]. Statistical Analyses Statistical analyses were carried out with SPSS software (version 26.0, SPSS Inc, Chicago, IL, USA). Data conforming to a normal distribution were denoted as mean ± standard deviation (SD). For comparison, t - tests or analysis of variance (ANOVA) were employed. Categorical data were shown as percentages and analyzed by the chi - square (χ²) test or Spearman test. Non - parametric data were presented as the median and compared using the Mann - Whitney test or Kruskal - Wallis test. Kaplan - Meier analysis along with log - rank testing was utilized to evaluate kidney survival. A two - tailed P value less than 0.05 was regarded as statistically significant, and 95% confidence intervals (CIs) were reported when appropriate. Ethics This research involving humans was approved by the Medical Ethics Committee of the Jinling Hospital (Approval No.2024DZKY-068-53), with informed consent waived due to the retrospective design. Results Baseline characteristics The baseline characteristics of the 374 eligible children were presented in Table 1 . In the GC + RASB group, there were 134 males and 96 females, yielding a male-to-female ratio of 1.40:1. In the RASB group, the numbers were 91 males and 53 females, with a male-to-female ratio of 1.72:1. The GC + RASB group exhibited significantly lower albumin levels and higher creatinine levels compared to the RASB group (both P < 0.05). However, no significant differences were observed between the two groups in terms of the prevalence of hypertension, SBP, DBP, triglycerides, cholesterol, UA, IgA, IgG, IgM, C3, eGFR, 24h-UP, uRBP, uC3, uNAG, and uα2-m (all P > 0.05). According to the Oxford Classification criteria, no significant differences were observed between the two groups with respect to Oxford Classification score and immunofluorescence deposition (all P > 0.05). Table 1 Comparison of general conditions of children with IgAN in two groups Characteristics GC + RASB(n = 230) RASB(n = 144) P value Female, n (%) 100(43.5) 53(36.8) 0.202 Age, yr 14.33 ± 3.24 13.42 ± 3.38 0.576 Hypertension(%) 41(17.83) 29(20.14) 0.577 Systolic BP, mmHg 118.90 ± 13.65 108.55 ± 1.65 0.934 Diastolic BP, mmHg 63.34 ± 8.40 61.73 ± 7.32 0.059 eGFR(ml/min/1.73m 2 ) 122.88 ± 4.12 123.46 ± 3.75 0.171 Creatinine(umol/L) 49.07 ± 7.15 46.44 ± 9.87 0.006 Uric acid(umol/L) 313.00(279.75,338.25) 310.5(286.25,346.75) 0.447 Serum albumin(g/L) 37.97 ± 8.52 40.48 ± 9.30 0.019 Cholesterol(mmol/L) 5.33 ± 2.46 5.39 ± 2.80 0.825 Triglycerides (umol/L) 1.45 ± 0.97 1.58 ± 0.94 0.200 Serum C3(g/L) 1.02(0.88,1.17) 1.03(0.87,1.22) 0.634 Serum IgA(g/L) 2.19(1.68, 3.01) 2.43(1.74,3.09) 0.390 Serum IgG(g/L) 8.08(5.05,10.70) 8.69(5.54,10.50) 0.596 Serum IgM(g/L) 1.11(0.83,1.59) 1.16(0.82,1.42) 0.441 Proteinuria(g/24h) 1.16(0.58,2.09) 0.83(0.56, 1.73) 0.172 uC3(mg/L) 2.31(2.00,3.22) 2.47(2.00, 3.28) 0.429 uα2-m(mg/L) 2.73(2.00,3.42) 2.97(2.00,3.64) 0.894 uNAG(u/g*cr) 16.40(8.80,28.25) 17.45(10.60,34.20) 0.104 uRBP(ug/mL) 0.17(0.10, 0.33) 0.20(0.10,0.40) 0.263 Oxford classification, n (%) M score 0.945 M0 178(77.39) 111(77.08) M1 52(22.61) 33(22.92) E score 0.678 E0 155(67.39) 100(69.44) E1 75(32.61) 44(30.56) S score 0.125 S0 143(62.17) 78(54.17) S1 87(37.83) 66(45.83) T score 0.512 T0 138(60.00) 103(71.53) T1 45(19.57) 37(25.69) T2 10(4.35) 4(2.78) C score 0.751 C0 135(58.70) 82(56.94) C1 86(37.39) 54(37.50) C2 9(3.91) 8(5.56) Immunofluorescence deposition, n (%) IgG deposition 44(19.13) 40(27.78) 0.051 IgM deposition 89(38.70) 62(43.06) 0.403 C3 deposition 183(79.57) 118(81.94) 0.572 C4 deposition 9(3.91) 4(2.78) 0.610 C1q deposition 9(3.91) 12(8.33) 0.076 Comparison of efficacy and adverse reactions between groups Throughout the follow-up period, the GC + RASB group exhibited a significantly higher proteinuria remission rate compared to the RASB group starting from 6 months of treatment, and this superiority persisted until the end of follow-up (all P < 0.05). At the follow-up endpoint, no significant difference was observed between the two groups regarding hematuria remission. In the GC + RASB group, adverse events included elevated blood glucose in 12 children, special site infections in 5 children (including 2 cases of cellulitis, 2 case of pulmonary tuberculosis, and 1 case of purulent meningitis), impaired liver function in 9 children, and central obesity in 21 children. When compared to the RASB group, a statistically significant difference was noted in the incidence of central obesity (9.13% vs. 0%, P = 0.001), as detailed in Table 2 . Table 2 Comparison of efficacy and adverse reactions between groups Characteristics GC + RASB group(n = 230) RASB group(n = 144) P value protein remission rate(%) 3 months a 74(32.17) 27(18.75) 0.040 6 months b 113(49.13) 35(24.31) <0.001 12 months c 154(66.96) 46(31.94) <0.001 24 months d 158(68.70) 57(39.58) <0.001 follow-up endpoint 198(86.09) 67(46.53) <0.001 hematuria remission (follow-up endpoint) 138(60.00) 73(50.70) 0.768 The primary endpoint(%) 12(5.22) 16(11.11) 0.035 ≥ 40% decline in eGFR 8(3.48) 12(8.33) 0.042 progression to kidney failure(%) 4(1.74) 4(2.78) 0.491 death caused by kidney diseases 0 0 NA Adverse reactions(%) central obesity 21(9.13) 0 <0.001 impaired liver function 9(3.91) 4(3.47) 0.560 special site infection e 5(2.17) 0 0.161 elevated blood glucose 12(5.22) 3(2.08) 0.178 Note: The protein remission timepoints include the initial 6-month treatment period. a 3 months refers to the assessment conducted halfway through the treatment period. b 6 months refers to the assessment at the end of the treatment period c 12 months refer to follow-up assessments after treatment completion. d 24 months refer to follow-up assessments after treatment completion. e special site infection including 2 cases of cellulitis, 2 case of pulmonary tuberculosis, and 1 case of purulent meningitis Effect of glucocorticoid therapy on the prognosis of children with IgAN The final follow-up was conducted on September 30, 2024. The median follow-up duration was 130.97 months (interquartile range: 101.58-168.65 months), during which a total of 28 endpoint events were recorded. In the GC + RASB group, 12 cases (5.22%) of IgAN endpoint events were observed, compared to 16 cases (11.11%) in the RASB group. This difference was statistically significant (P = 0.035). Kaplan-Meier survival analysis revealed that the cumulative survival rates for IgAN patients in the GC + RASB group at 50, 100, 150, and 200 months were 99.1%, 98.6%, 96.6%, and 88.3%, respectively. In contrast, the corresponding cumulative kidney survival rates in the RASB group were 99.30%, 96.90%, 89.90%, and 70.50%, respectively. The difference in cumulative survival rates between the two groups was statistically significant (Log-rank test: χ²=5.245, P = 0.022, Fig. A). When stratified by eGFR levels, a significant difference in cumulative survival rates between the two groups was observed when eGFR was > 50 ml/min/1.73 m² (Log-rank test: χ²=5.120, P = 0.024, Fig. B). However, no significant difference was noted when eGFR was ≤ 50 ml/min/1.73 m² (Log-rank test: χ²=0.017, P = 0.897, Fig. C). In terms of 24h-UP levels, no significant difference in cumulative survival rates was found between the two groups when 24h-UP was < 1 g/d (Log-rank test: χ²=0.065, P = 0.798, Fig. D). However, significant differences were observed when 24h-UP was ≥ 1 g/d and 50 ml/min/1.73 m² and 24h-UP was ≥ 1 g/d, a significant difference in cumulative kidney survival was observed (Log-rank test: χ²=4.046, P = 0.044,Fig. G). Conversely, no significant difference was noted when eGFR was ≤ 50 ml/min/1.73 m² and 24h-UP was < 1 g/d (Log-rank test: χ²=0.364, P = 0.546, Fig. H). Discussion At the outset of the study, individuals in the GC+RASB group presented with higher serum creatinine and lower plasma albumin levels than those in the RASB group. The increased serum creatinine suggests a decline in renal function. Meanwhile, the reduced plasma albumin may point to substantial proteinuria or compromised liver function. These observations underscore the greater renal impairment and potential nutritional deficits in the GC+RASB group at the outset of the study. In terms of pathological manifestations, there were no obvious differences between two groups, which proved that the two groups were comparable. This finding is consistent with the results of The Validation Study of the Oxford Classification of IgA nephropathy (VALIGA)[23], which demonstrated that the MEST-C score was almost identical in both the conservative and intervention groups. Specifically, the percentages of M, E, S, Tand C were similar between the two groups, indicating that the pathological features were well-balanced. At the follow-up endpoint, a significant difference in the complete remission rate of proteinuria was noted between the two groups (86.09% in the GC+RASB group vs. 46.53% in the RASB group, P <0.001). This result underscores the superior efficacy of GC combined with RASB in achieving proteinuria remission. Children who develop ESKD face a significantly reduced life expectancy, averaging 19 years after starting dialysis and around 40 years following kidney transplantation [24]. This stark reality may explain why pediatricians often prescribe steroids in addition to ACE inhibitors or ARBs, aiming to achieve complete remission of the disease[25]. Regarding adverse events, children in the GC+RASB group were more likely to develop central obesity compared to those in the RASB group. However, this effect resolved after discontinuation of GC therapy, demonstrating the relative safety of GC in pediatric IgAN patients. A recent randomized controlled trial[26] in adults demonstrated that an enteric-coated, extended-release formulation of budesonide significantly reduced proteinuria and stabilized eGFR. This finding provides further evidence for the role of mucosal immunity in IgAN pathogenesis and suggests that targeted mucosal therapies may reduce the need for systemic immunosuppression. This approach represents a promising future direction for the treatment of IgAN. The 200-month cumulative kidney survival rate in the GC+RASB group was 88.3%, significantly higher than the 70.5% observed in the RASB group. This finding indicates that GC treatment can effectively delay disease progression in IgAN. Further stratified analysis revealed that GC therapy significantly reduced the risk of progression to ESRD in children with an initial eGFR > 50 ml/min/1.73 m² and proteinuria ≥1 g/d. Conversely, for patients with an initial eGFR ≤ 50 ml/min/1.73m² or proteinuria <1 g/d, GC therapy didn’t provide additional benefits in terms of kidney survival. Our study aligns with both the KDIGO guidelines[9] and the recent IPNA guidelines[27] for pediatric IgAN, which recommend combining GC with RASB for children with proteinuria >1 g/day. Our findings confirm the effectiveness of this combined therapy in reducing proteinuria and improving kidney outcomes. Second, our study found no significant differences in MEST-C scores between the two groups. This suggests that kidney biopsy may not be necessary for deciding when or if to initiate GC therapy in IgAN patients. The MEST-C score, while useful for prognostic staging, didn’t predict the response to GC therapy in our cohort. Third, the long follow-up period in our study, with all children followed for over 5 years and a median follow-up duration of over 10 years, provides robust data on kidney outcomes. This extended follow-up period is crucial for accurately assessing the long-term effects of treatment and disease progression in pediatric IgAN patients. Nevertheless, several studies have indicated that immunosuppressive therapy can still be effective in individuals with advanced chronic kidney disease. For example, Tesar et al.[23] found that GC reduced the risk of progression to ESKD in IgAN patients with an eGFR ≤50 mL/min/1.73 m². Similarly, Stangou [28]and Pozzi[29] showed that GC improved proteinuria and delayed kidney function decline in patients with an eGFR <30 mL/min/1.73 m². The differences in outcomes may be due to the higher prevalence of IgAN and faster eGFR decline in East Asia (China), as well as the shorter follow-up periods in the Stangou and Pozzi studies compared to ours. Due to the prolonged follow-up duration in this study, evaluating drug tapering or the total GC dose was impractical. Additionally, the selection of treatment regimens was not based on a strict, predefined single criterion. Instead, it was determined by clinicians after a comprehensive evaluation of each patient's clinical characteristics and pathological manifestations. Given the single-center, observational, and retrospective nature of this study, it is challenging to completely eliminate residual confounding factors. Although we made every effort to control for known confounding factors in our analysis, we cannot completely rule out the potential impact of selection bias and residual confounding on the results. We have emphasized these limitations and suggest that future studies could further validate our findings through more rigorous study designs, such as prospective cohort studies or randomized controlled trials. In conclusion，this study found that GC therapy can delay disease progression in children with IgAN. However, the benefits of GC treatment were only evident in pediatric IgAN who had an initial eGFR ＞50 ml/min/1.73 m² and proteinuria levels≥ 1 g/d. In contrast, for children with an initial eGFR＜50 ml/min/1.73 m², or with proteinuria＜1 g/d, adding GC therapy did not significantly improve cumulative kidney survival outcomes. Declarations Data availability Deidentified individual participant’s data will not be made available. Acknowledgements We would like to thank everyone involved in data collection, including all the parents for their cooperation in this study. Funding This work was supported by funds from Shenzhen Science and Technology Program (No. JCYJ20220530145001002). Author information Authors and Affiliations Department of Pediatric Intensive Care Unit, The Seventh Affiliated Hospital，Sun Yat-sen University, 628 Zhenyuan Road, Guangming District, Shenzhen,518107,China Heyan Wu, Lidan Zhang Department of Pediatrics, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China Zhengkun Xia Corresponding author Correspondence to Zhengkun Xia and Lidan Zhang Ethics declarations Conflict of interest The authors declare no competing interests. References Moriyama, T., Tanaka, K., Iwasaki, C., Oshima, Y., Ochi, A., Kataoka, H., Itabashi, M., Takei, T., Uchida, K., & Nitta, K. (2014). Prognosis in IgA nephropathy: 30-year analysis of 1,012 patients at a single center in Japan. PloS one, 9(3), e91756. https://doi.org/10.1371/journal.pone.0091756 Wyatt, R. J., Kritchevsky, S. B., Woodford, S. Y., Miller, P. M., Roy, S., 3rd, Holland, N. H., Jackson, E., & Bishof, N. A. (1995). IgA nephropathy: long-term prognosis for pediatric patients. The Journal of pediatrics, 127(6), 913–919. https://doi.org/10.1016/s0022-3476(95)70027-7 Yata, N., Nakanishi, K., Shima, Y., Togawa, H., Obana, M., Sako, M., Nozu, K., Tanaka, R., Iijima, K., & Yoshikawa, N. (2008). Improved renal survival in Japanese children with IgA nephropathy. Pediatric nephrology (Berlin, Germany), 23(6), 905–912. https://doi.org/10.1007/s00467-007-0726-5 Suzuki, H., Kiryluk, K., Novak, J., Moldoveanu, Z., Herr, A. B., Renfrow, M. B., Wyatt, R. J., Scolari, F., Mestecky, J., Gharavi, A. G., & Julian, B. A. (2011). The pathophysiology of IgA nephropathy. Journal of the American Society of Nephrology : JASN, 22(10), 1795–1803. https://doi.org/10.1681/ASN.2011050464 Bagchi, S., Mani, K., Swamy, A., Barwad, A., Singh, G., Bhowmik, D., & Agarwal, S. K. (2021). Supportive Management of IgA Nephropathy With Renin-Angiotensin Blockade, the AIIMS Primary IgA Nephropathy Cohort (APPROACH) Study. Kidney international reports, 6(6), 1661–1668. https://doi.org/10.1016/j.ekir.2021.02.018 Coppo, R., Amore, A., Gianoglio, B., Cacace, G., Picciotto, G., Roccatello, D., Peruzzi, L., Piccoli, G., & De Filippi, P. G. (1993). Angiotensin II local hyperreactivity in the progression of IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation, 21(6), 593–602. https://doi.org/10.1016/s0272-6386(12)80031-x Tanaka, S., Ninomiya, T., Katafuchi, R., Masutani, K., Nagata, M., Tsuchimoto, A., Hirakata, H., Kitazono, T., & Tsuruya, K. (2016). The effect of renin-angiotensin system blockade on the incidence of end-stage renal disease in IgA nephropathy. Clinical and experimental nephrology, 20(5), 689–698. https://doi.org/10.1007/s10157-015-1195-y Tunnicliffe, D. J., Reid, S., Craig, J. C., Samuels, J. A., Molony, D. A., & Strippoli, G. F. (2024). Non-immunosuppressive treatment for IgA nephropathy. The Cochrane database of systematic reviews, 2(2), CD003962. https://doi.org/10.1002/14651858.CD003962.pub3 Stevens, P. E., Levin, A., & Kidney Disease: Improving Global Outcomes Chronic Kidney Disease Guideline Development Work Group Members (2013). Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Annals of internal medicine, 158(11), 825–830. https://doi.org/10.7326/0003-4819-158-11-201306040-00007 Kobayashi, Y., Fujii, K., Hiki, Y., & Tateno, S. (1986). Steroid therapy in IgA nephropathy: a prospective pilot study in moderate proteinuric cases. The Quarterly journal of medicine, 61(234), 935–943. Kobayashi, Y., Fujii, K., Hiki, Y., Tateno, S., Kurokawa, A., & Kamiyama, M. (1988). Steroid therapy in IgA nephropathy: a retrospective study in heavy proteinuric cases. Nephron, 48(1), 12–17. https://doi.org/10.1159/000184861 Pozzi, C., Bolasco, P. G., Fogazzi, G. B., Andrulli, S., Altieri, P., Ponticelli, C., & Locatelli, F. (1999). Corticosteroids in IgA nephropathy: a randomised controlled trial. Lancet (London, England), 353(9156), 883–887. https://doi.org/10.1016/s0140-6736(98)03563-6 Rauen, T., Eitner, F., Fitzner, C., Sommerer, C., Zeier, M., Otte, B., Panzer, U., Peters, H., Benck, U., Mertens, P. R., Kuhlmann, U., Witzke, O., Gross, O., Vielhauer, V., Mann, J. F., Hilgers, R. D., Floege, J., & STOP-IgAN Investigators (2015). Intensive Supportive Care plus Immunosuppression in IgA Nephropathy. The New England journal of medicine, 373(23), 2225–2236. https://doi.org/10.1056/NEJMoa1415463 Lv, J., Zhang, H., Wong, M. G., Jardine, M. J., Hladunewich, M., Jha, V., Monaghan, H., Zhao, M., Barbour, S., Reich, H., Cattran, D., Glassock, R., Levin, A., Wheeler, D., Woodward, M., Billot, L., Chan, T. M., Liu, Z. H., Johnson, D. W., Cass, A., … TESTING Study Group (2017). Effect of Oral Methylprednisolone on Clinical Outcomes in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA, 318(5), 432–442. https://doi.org/10.1001/jama.2017.9362 Coppo, R., Lofaro, D., Camilla, R. R., Bellur, S., Cattran, D., Cook, H. T., Roberts, I. S., Peruzzi, L., Amore, A., Emma, F., Fuiano, L., Berg, U., Topaloglu, R., Bilginer, Y., Gesualdo, L., Polci, R., Mizerska-Wasiak, M., Caliskan, Y., Lundberg, S., Cancarini, G., … Honsova, E. (2017). Erratum to: Risk factors for progression in children and young adults with IgA nephropathy: an analysis of 261 cases from the VALIGA European cohort. Pediatric nephrology (Berlin, Germany), 32(1), 193–194. https://doi.org/10.1007/s00467-016-3506-2 Lv, J., Wong, M. G., Hladunewich, M. A., Jha, V., Hooi, L. S., Monaghan, H., Zhao, M., Barbour, S., Jardine, M. J., Reich, H. N., Cattran, D., Glassock, R., Levin, A., Wheeler, D. C., Woodward, M., Billot, L., Stepien, S., Rogers, K., Chan, T. M., Liu, Z. H., … TESTING Study Group (2022). Effect of Oral Methylprednisolone on Decline in Kidney Function or Kidney Failure in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA, 327(19), 1888–1898. https://doi.org/10.1001/jama.2022.5368 Schwartz, G. J., Muñoz, A., Schneider, M. F., Mak, R. H., Kaskel, F., Warady, B. A., & Furth, S. L. (2009). New equations to estimate GFR in children with CKD. Journal of the American Society of Nephrology : JASN, 20(3), 629–637. https://doi.org/10.1681/ASN.2008030287 Chi, X. H., Li, G. P., Wang, Q. S., Qi, Y. S., Huang, K., Zhang, Q., & Xue, Y. M. (2017). CKD-EPI creatinine-cystatin C glomerular filtration rate estimation equation seems more suitable for Chinese patients with chronic kidney disease than other equations. BMC nephrology, 18(1), 226. https://doi.org/10.1186/s12882-017-0637-z Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group (2021). KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney international, 100(4S), S1–S276. https://doi.org/10.1016/j.kint.2021.05.021 de Simone, G., Mancusi, C., Hanssen, H., Genovesi, S., Lurbe, E., Parati, G., Sendzikaite, S., Valerio, G., Di Bonito, P., Di Salvo, G., Ferrini, M., Leeson, P., Moons, P., Weismann, C. G., & Williams, B. (2022). Hypertension in children and adolescents. European heart journal, 43(35), 3290–3301. https://doi.org/10.1093/eurheartj/ehac328 Trimarchi, H., Barratt, J., Cattran, D. C., Cook, H. T., Coppo, R., Haas, M., Liu, Z. H., Roberts, I. S., Yuzawa, Y., Zhang, H., Feehally, J., IgAN Classification Working Group of the International IgA Nephropathy Network and the Renal Pathology Society, & Conference Participants (2017). Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney international, 91(5), 1014–1021. https://doi.org/10.1016/j.kint.2017.02.003 Shima, Y., Nakanishi, K., Hama, T., Mukaiyama, H., Sato, M., Tanaka, Y., Tanaka, R., Kaito, H., Nozu, K., Sako, M., Iijima, K., & Yoshikawa, N. (2020). Crescentic IgA nephropathy in children. Pediatric nephrology (Berlin, Germany), 35(6), 1005–1014. https://doi.org/10.1007/s00467-020-04483-w Tesar, V., Troyanov, S., Bellur, S., Verhave, J. C., Cook, H. T., Feehally, J., Roberts, I. S., Cattran, D., Coppo, R., & VALIGA study of the ERA-EDTA Immunonephrology Working Group (2015). Corticosteroids in IgA Nephropathy: A Retrospective Analysis from the VALIGA Study. Journal of the American Society of Nephrology : JASN , 26 (9), 2248–2258. https://doi.org/10.1681/ASN.2014070697 Mitsnefes, M. M., Laskin, B. L., Dahhou, M., Zhang, X., & Foster, B. J. (2013). Mortality risk among children initially treated with dialysis for end-stage kidney disease, 1990-2010. JAMA , 309 (18), 1921–1929. https://doi.org/10.1001/jama.2013.4208 Cambier, A., Boyer, O., Deschenes, G., Gleeson, J., Couderc, A., Hogan, J., & Robert, T. (2020). Steroid therapy in children with IgA nephropathy. Pediatric nephrology (Berlin, Germany) , 35 (3), 359–366. https://doi.org/10.1007/s00467-018-4189-7 Fellström, B. C., Barratt, J., Cook, H., Coppo, R., Feehally, J., de Fijter, J. W., Floege, J., Hetzel, G., Jardine, A. G., Locatelli, F., Maes, B. D., Mercer, A., Ortiz, F., Praga, M., Sørensen, S. S., Tesar, V., Del Vecchio, L., & NEFIGAN Trial Investigators (2017). Targeted-release budesonide versus placebo in patients with IgA nephropathy (NEFIGAN): a double-blind, randomised, placebo-controlled phase 2b trial. Lancet (London, England), 389(10084), 2117–2127. https://doi.org/10.1016/S0140-6736(17)30550-0 Vivarelli, M., Samuel, S., Coppo, R., Barratt, J., Bonilla-Felix, M., Haffner, D., Gibson, K., Haas, M., Abdel-Hafez, M. A., Adragna, M., Brogan, P., Kim, S., Liu, I., Liu, Z. H., Mantan, M., Shima, Y., Shimuzu, M., Shen, Q., Trimarchi, H., Hahn, D., … International Pediatric Nephrology Association (2025). IPNA clinical practice recommendations for the diagnosis and management of children with IgA nephropathy and IgA vasculitis nephritis. Pediatric nephrology (Berlin, Germany), 40(2), 533–569. https://doi.org/10.1007/s00467-024-06502-6 Stangou, M., Ekonomidou, D., Giamalis, P., Liakou, H., Tsiantoulas, A., Pantzaki, A., Papagianni, A., Efstratiadis, G., Alexopoulos, E., & Memmos, D. (2011). Steroids and azathioprine in the treatment of IgA nephropathy. Clinical and experimental nephrology, 15(3), 373–380. https://doi.org/10.1007/s10157-011-0415-3 Pozzi C. (2016). Treatment of IgA nephropathy. Journal of nephrology, 29(1), 21–25. https://doi.org/10.1007/s40620-015-0248-3 Supplementary Files GraphicalAbstract.pptx Cite Share Download PDF Status: Published Journal Publication published 15 Jul, 2025 Read the published version in Pediatric Nephrology → Version 1 posted Reviewers agreed at journal 23 Apr, 2025 Reviewers invited by journal 20 Apr, 2025 Editor assigned by journal 20 Apr, 2025 First submitted to journal 19 Apr, 2025 Editorial decision: Minor Revisions Needed 03 Mar, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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-5996564","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":445380178,"identity":"692b4a57-4a90-418f-97af-8068608a496f","order_by":0,"name":"Heyan Wu","email":"","orcid":"","institution":"Pediatric Intensive Care Unit,The Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":false,"prefix":"","firstName":"Heyan","middleName":"","lastName":"Wu","suffix":""},{"id":445380179,"identity":"c68ad067-8a35-4af8-b86d-1a36183d1f37","order_by":1,"name":"Zhengkun Xia","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAp0lEQVRIiWNgGAWjYFCCAwyMDRUScvwkajljYSzZQIo9jI1tFYkbiNZiznjG+OPMeRKMGxiYHz66QYwWy4ZjCYYbt0kwmzOwGRvnEKPF4MDhA4kPt0mwWTbwsEkTqeVgw8GHcyR4DA4Qr+XwwcaNDRISpGg5lsw445iEgWQz0X65AQyxnpq6+n725oePidLCIHEAymAmSjkI8DcQrXQUjIJRMApGKgAAsQM0QnMHlQcAAAAASUVORK5CYII=","orcid":"","institution":"Department of Pediatrics，Jinling Hospital","correspondingAuthor":true,"prefix":"","firstName":"Zhengkun","middleName":"","lastName":"Xia","suffix":""},{"id":445380180,"identity":"7a6f5d51-e64c-4db9-993a-03c92117f442","order_by":2,"name":"Lidan Zhang","email":"","orcid":"","institution":"Pediatric Intensive Care Unit，The Seventh Affiliated Hospital of Sun Yat-sen University","correspondingAuthor":false,"prefix":"","firstName":"Lidan","middleName":"","lastName":"Zhang","suffix":""}],"badges":[],"createdAt":"2025-02-10 07:23:00","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-5996564/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-5996564/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1007/s00467-025-06845-8","type":"published","date":"2025-07-15T15:57:32+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":81544013,"identity":"c7a6fff6-95f4-4070-950c-57b395d61f18","added_by":"auto","created_at":"2025-04-28 11:28:04","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":453894,"visible":true,"origin":"","legend":"\u003cp\u003eLegend not included with this version.\u003c/p\u003e","description":"","filename":"Figure1.png","url":"https://assets-eu.researchsquare.com/files/rs-5996564/v1/7472daa5047457ca06b9e5e0.png"},{"id":87219547,"identity":"acda48e8-eefd-47eb-b24c-cca628fb45bc","added_by":"auto","created_at":"2025-07-21 16:05:17","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1087091,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-5996564/v1/ab516053-7768-4a0a-9ddc-d1a3bd38dee7.pdf"},{"id":81544027,"identity":"d404b53b-31d0-4db8-b0ce-d6156745f849","added_by":"auto","created_at":"2025-04-28 11:28:05","extension":"pptx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":4934952,"visible":true,"origin":"","legend":"","description":"","filename":"GraphicalAbstract.pptx","url":"https://assets-eu.researchsquare.com/files/rs-5996564/v1/3d0e6b7e3e4fd16b45c99585.pptx"}],"financialInterests":"","formattedTitle":"Retrospective Analysis of Glucocorticoid Therapy in Pediatric immunoglobulin A Nephropathy: Kidney Outcomes and Efficacy","fulltext":[{"header":"Introduction","content":"\u003cp\u003eImmunoglobulin A nephropathy (IgAN) is a major cause of chronic glomerulonephritis in East Asia and represents a global health issue affecting both pediatric and adult populations. In adults, 1\u0026ndash;2% progress to end-stage kidney disease (ESKD) annually, and approximately 50% reach kidney failure within 20\u0026ndash;30 years[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. The prognosis for childhood IgAN is as severe as in adults, with 10\u0026ndash;13% of pediatric patients progressing to ESKD within 10 years of follow-up and 20\u0026ndash;30% doing so within 20 years [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The pathogenesis of IgAN is characterized by immune dysregulation mediated by aberrantly glycosylated IgA1 in the hinge region[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eRenin-angiotensin system blockers (RASB) have established renoprotective effects in both adult and pediatric IgAN and are considered first-line therapy. Multiple studies in adults, like the APPROACH study[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e], have demonstrated the efficacy of RASB in reducing proteinuria and potentially delaying disease progression. In children, although data are more limited, studies support the use of RASB based on the similar underlying pathophysiological mechanisms related to renin-angiotensin system activation in IgAN[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eHowever, glucocorticoid (GC) efficacy remains controversial[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. According to the KDIGO guidelines[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e], GC should be restricted to IgAN patients with persistent proteinuria and preserved renal function, while other immunosuppressants are generally discouraged. GC therapy has shown efficacy in reducing proteinuria and slowing renal function decline in IgAN, as evidenced by multiple clinical trials[\u003cspan additionalcitationids=\"CR11\" citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]had demonstrated that GC treatment can diminish proteinuria and postpone kidney function deterioration in IgAN. On the other hand, trials like the STOP - IgAN trial[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e], which showed that immunosuppressive treatment including GC can reduce proteinuria yet there was no difference in 3 - year renal function endpoints, had raised concerns about the long -term benefits. The TESTING study[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e] showed that a reduced-dose glucocorticoid regimen had similar effects on reducing proteinuria and protecting renal function as a full-dose regimen but with significantly fewer adverse effects. In the pediatric population, the situation is more complex. The use of GC in pediatric IgAN is based on the assumption that the underlying immune - mediated pathogenesis is similar to adults. However, due to the potential impact of GC on growth and development in children, the decision - making process is more challenging. The Validation Study of the Oxford Classification of IgA nephropathy (VALIGA) [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]showed that children\u0026thinsp;\u0026lt;\u0026thinsp;16 years treated with GC had a significantly reduced risk of progression towards ESKD. But the overall evidence base is still not as robust as in adults, and long-term follow-up studies are needed to assess potential impacts on growth and the developing immune system. Given these considerations, further research is needed to explore the impact of GCs on the prognosis of children with IgAN. Understanding the balance between the benefits and risks of GC therapy in this population is crucial for optimizing individualized treatment strategies. This study aims to improve the understanding of pediatric IgAN and provide a theoretical foundation for more effective and safer clinical management.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy design and participants\u003c/h2\u003e \u003cp\u003eThis retrospective cohort study evaluated pediatric patients (\u0026le;\u0026thinsp;18 years) with biopsy-proven IgAN treated at Jinling Hospital between January 2000 and December 2020.Eligible participants were stratified into two treatment groups based on the use of glucocorticoids: the RASB monotherapy group (RASB group) and the GC combined with RASB therapy group (GC\u0026thinsp;+\u0026thinsp;RASB group). We excluded patients with any of the following: (1) secondary IgA nephropathy (e.g., due to chronic liver disease, rheumatoid arthritis, Henoch-Sch\u0026ouml;nlein purpura, or ankylosing spondylitis);(2) indications for intensive glucocorticoid therapy (e.g., crescentic IgAN); (3) contraindications to GC(e.g., severe infections, active tuberculosis, malignancy, or uncontrolled hypertension);(4) use of other immunosuppressive agents within 1 year before or after treatment; (5) acute kidney injury or other causes of unstable renal function. All participants were followed for at least two years, with final follow-up data collected through September 30, 2024.\u003c/p\u003e \u003cp\u003eOur study was a retrospective analysis, and the selected patients were divided into two groups based on their prior treatment regimens. In clinical practice, the decision to use GC\u0026thinsp;+\u0026thinsp;RASB or RASB alone was primarily based on a combination of clinical judgment and biopsy results. Specifically, patients with more severe histological changes (such as higher degrees of glomerulosclerosis or more pronounced interstitial fibrosis) and higher levels of proteinuria were more likely to be treated with GC\u0026thinsp;+\u0026thinsp;RASB. Conversely, patients with milder pathological changes and lower levels of proteinuria were more often treated with RASB alone. Oral GC was initiated at 1 mg/kg/day (max 60 mg/day) for 4\u0026ndash;6 weeks, then tapered by 5 mg every 2 weeks until reaching 0.5 mg/kg/day, followed by a reduction of 2.5-5 mg every 2\u0026ndash;4 weeks until discontinuation, with a total treatment duration of 6 months.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eData collection\u003c/h3\u003e\n\u003cp\u003eThe study utilized retrospective medical record data from this patient cohort, with all follow-up information current through September 2024. Collected clinical parameters encompassed demographic characteristics (sex and age at diagnosis) and therapeutic interventions. Hemodynamic assessment incorporated mean arterial pressure (MAP), Systolic blood pressure (SBP) and Diastolic blood pressure (DBP). Longitudinal monitoring included treatment response evaluation, renal outcomes, and immunosuppressive regimen details. Biological specimens (blood and urine) were obtained concurrently with renal biopsy procedures. Serum markers: Albumin (Alb), lipid profile (cholesterol and triglycerides), uric acid(UA), serum immunoglobulin levels (IgG, IgA, IgM), complement 3 (C3), and renal function parameters [estimated glomerular filtration rate(eGFR) and serum creatinine (Scr)]. Urinary biomarkers:24-hour urinary protein(24h-UP), urinary α-2-macroglobulin(uα2-m), urinary N-acetyl-β-D-glucosaminidase (uNAG), urinary retinol-binding protein(uRBP), and urine complement3(uC3).\u003c/p\u003e\n\u003ch3\u003eOutcomes\u003c/h3\u003e\n\u003cp\u003eThe primary composite endpoint consisted of a\u0026thinsp;\u0026ge;\u0026thinsp;40% decline in eGFR from the baseline, progression to kidney failure (which was defined as the need for maintenance dialysis or kidney transplantation), or death caused by kidney disease, and this is consistent with that in The TESTING Randomized Clinical Trial[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. The safety endpoint recorded adverse events related to GC, including episodes of infection, hepatic dysfunction, central obesity, and hyperglycemia.\u003c/p\u003e\n\u003ch3\u003eDefinitions\u003c/h3\u003e\n\u003cp\u003eThe eGFR was calculated using the Schwartz formula[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e] or CKD-EPI equation[\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e] (\u0026gt;\u0026thinsp;16 years)],. We quantified the rate of eGFR decline during the follow-up period. Complete proteinuria remission was defined as a 24-hour urine protein excretion\u0026thinsp;\u0026lt;\u0026thinsp;200 mg/day for pediatric patients, consistent with the KDIGO Clinical Practice Guidelines for Glomerular Diseases[\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. Children were considered to have hypertension if their systolic or diastolic blood pressure continuously exceeds the 95th percentile of children of the same age, gender, and height[\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e].Mean arterial pressure (MAP), derived using the standard formula: [(SBP\u0026thinsp;+\u0026thinsp;2 \u0026times; DBP)/3]. Renal biopsy specimens were graded based on the Oxford Classification[\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. Crescentic IgAN was defined as IgAN with more than 50% of glomeruli showing crescents[\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e].\u003c/p\u003e\n\u003ch3\u003eStatistical Analyses\u003c/h3\u003e\n\u003cp\u003eStatistical analyses were carried out with SPSS software (version 26.0, SPSS Inc, Chicago, IL, USA). Data conforming to a normal distribution were denoted as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation (SD). For comparison, t - tests or analysis of variance (ANOVA) were employed. Categorical data were shown as percentages and analyzed by the chi - square (χ\u0026sup2;) test or Spearman test. Non - parametric data were presented as the median and compared using the Mann - Whitney test or Kruskal - Wallis test. Kaplan - Meier analysis along with log - rank testing was utilized to evaluate kidney survival. A two - tailed P value less than 0.05 was regarded as statistically significant, and 95% confidence intervals (CIs) were reported when appropriate.\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eEthics\u003c/h2\u003e \u003cp\u003eThis research involving humans was approved by the Medical Ethics Committee of the Jinling Hospital (Approval No.2024DZKY-068-53), with informed consent waived due to the retrospective design.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec10\" class=\"Section2\"\u003e \u003ch2\u003eBaseline characteristics\u003c/h2\u003e \u003cp\u003eThe baseline characteristics of the 374 eligible children were presented in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. In the GC\u0026thinsp;+\u0026thinsp;RASB group, there were 134 males and 96 females, yielding a male-to-female ratio of 1.40:1. In the RASB group, the numbers were 91 males and 53 females, with a male-to-female ratio of 1.72:1. The GC\u0026thinsp;+\u0026thinsp;RASB group exhibited significantly lower albumin levels and higher creatinine levels compared to the RASB group (both \u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.05). However, no significant differences were observed between the two groups in terms of the prevalence of hypertension, SBP, DBP, triglycerides, cholesterol, UA, IgA, IgG, IgM, C3, eGFR, 24h-UP, uRBP, uC3, uNAG, and uα2-m (all \u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026gt;\u0026thinsp;0.05). According to the Oxford Classification criteria, no significant differences were observed between the two groups with respect to Oxford Classification score and immunofluorescence deposition (all \u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026gt;\u0026thinsp;0.05).\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\u003eComparison of general conditions of children with IgAN in two groups\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCharacteristics\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eGC\u0026thinsp;+\u0026thinsp;RASB(n\u0026thinsp;=\u0026thinsp;230)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eRASB(n\u0026thinsp;=\u0026thinsp;144)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\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\u003eFemale, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e100(43.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e53(36.8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.202\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAge, yr\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e14.33\u0026thinsp;\u0026plusmn;\u0026thinsp;3.24\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e13.42\u0026thinsp;\u0026plusmn;\u0026thinsp;3.38\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.576\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHypertension(%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e41(17.83)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e29(20.14)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.577\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSystolic BP, mmHg\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e118.90\u0026thinsp;\u0026plusmn;\u0026thinsp;13.65\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e108.55\u0026thinsp;\u0026plusmn;\u0026thinsp;1.65\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.934\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDiastolic BP, mmHg\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e63.34\u0026thinsp;\u0026plusmn;\u0026thinsp;8.40\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e61.73\u0026thinsp;\u0026plusmn;\u0026thinsp;7.32\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.059\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eeGFR(ml/min/1.73m\u003csup\u003e2\u003c/sup\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e122.88\u0026thinsp;\u0026plusmn;\u0026thinsp;4.12\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e123.46\u0026thinsp;\u0026plusmn;\u0026thinsp;3.75\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.171\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCreatinine(umol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e49.07\u0026thinsp;\u0026plusmn;\u0026thinsp;7.15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e46.44\u0026thinsp;\u0026plusmn;\u0026thinsp;9.87\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.006\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eUric acid(umol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e313.00(279.75,338.25)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e310.5(286.25,346.75)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.447\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum albumin(g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e37.97\u0026thinsp;\u0026plusmn;\u0026thinsp;8.52\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e40.48\u0026thinsp;\u0026plusmn;\u0026thinsp;9.30\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.019\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCholesterol(mmol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e5.33\u0026thinsp;\u0026plusmn;\u0026thinsp;2.46\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e5.39\u0026thinsp;\u0026plusmn;\u0026thinsp;2.80\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.825\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTriglycerides (umol/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e1.45\u0026thinsp;\u0026plusmn;\u0026thinsp;0.97\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.58\u0026thinsp;\u0026plusmn;\u0026thinsp;0.94\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.200\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum C3(g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e1.02(0.88,1.17)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.03(0.87,1.22)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.634\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum IgA(g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e2.19(1.68, 3.01)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e2.43(1.74,3.09)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.390\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum IgG(g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e8.08(5.05,10.70)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e8.69(5.54,10.50)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.596\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum IgM(g/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e1.11(0.83,1.59)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.16(0.82,1.42)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.441\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eProteinuria(g/24h)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e1.16(0.58,2.09)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e0.83(0.56, 1.73)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.172\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003euC3(mg/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e2.31(2.00,3.22)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e2.47(2.00, 3.28)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.429\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003euα2-m(mg/L)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e2.73(2.00,3.42)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e2.97(2.00,3.64)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.894\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003euNAG(u/g*cr)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e16.40(8.80,28.25)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e17.45(10.60,34.20)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.104\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003euRBP(ug/mL)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e0.17(0.10, 0.33)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e0.20(0.10,0.40)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.263\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eOxford classification, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eM score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.945\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eM0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e178(77.39)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e111(77.08)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eM1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e52(22.61)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e33(22.92)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eE score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.678\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eE0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e155(67.39)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e100(69.44)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eE1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e75(32.61)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e44(30.56)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eS score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.125\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eS0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e143(62.17)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e78(54.17)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eS1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e87(37.83)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e66(45.83)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eT score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.512\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eT0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e138(60.00)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e103(71.53)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eT1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e45(19.57)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e37(25.69)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eT2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e10(4.35)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e4(2.78)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC score\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.751\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e135(58.70)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e82(56.94)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e86(37.39)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e54(37.50)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e9(3.91)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e8(5.56)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eImmunofluorescence deposition, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIgG deposition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e44(19.13)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e40(27.78)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.051\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIgM deposition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e89(38.70)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e62(43.06)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.403\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC3 deposition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e183(79.57)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e118(81.94)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.572\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC4 deposition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e9(3.91)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e4(2.78)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.610\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eC1q deposition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e9(3.91)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e12(8.33)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e0.076\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec11\" class=\"Section2\"\u003e \u003ch2\u003eComparison of efficacy and adverse reactions between groups\u003c/h2\u003e \u003cp\u003eThroughout the follow-up period, the GC\u0026thinsp;+\u0026thinsp;RASB group exhibited a significantly higher proteinuria remission rate compared to the RASB group starting from 6 months of treatment, and this superiority persisted until the end of follow-up (all \u003cem\u003eP\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.05). At the follow-up endpoint, no significant difference was observed between the two groups regarding hematuria remission. In the GC\u0026thinsp;+\u0026thinsp;RASB group, adverse events included elevated blood glucose in 12 children, special site infections in 5 children (including 2 cases of cellulitis, 2 case of pulmonary tuberculosis, and 1 case of purulent meningitis), impaired liver function in 9 children, and central obesity in 21 children. When compared to the RASB group, a statistically significant difference was noted in the incidence of central obesity (9.13% vs. 0%, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.001), as detailed in Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\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\u003eComparison of efficacy and adverse reactions between groups\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\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 \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCharacteristics\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eGC\u0026thinsp;+\u0026thinsp;RASB group(n\u0026thinsp;=\u0026thinsp;230)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eRASB group(n\u0026thinsp;=\u0026thinsp;144)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\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\u003eprotein remission rate(%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e3 months\u003csup\u003ea\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e74(32.17)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e27(18.75)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.040\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e6 months\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e113(49.13)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e35(24.31)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e12 months\u003csup\u003ec\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e154(66.96)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e46(31.94)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e24 months\u003csup\u003ed\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e158(68.70)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e57(39.58)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003efollow-up endpoint\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e198(86.09)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e67(46.53)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ehematuria remission (follow-up endpoint)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e138(60.00)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e73(50.70)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.768\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eThe primary endpoint(%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e12(5.22)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e16(11.11)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.035\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;40% decline in eGFR\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e8(3.48)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e12(8.33)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.042\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eprogression to kidney failure(%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4(1.74)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e4(2.78)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.491\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003edeath caused by kidney diseases\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eNA\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAdverse reactions(%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ecentral obesity\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21(9.13)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u0026lt;0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eimpaired liver function\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e9(3.91)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e4(3.47)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.560\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003especial site infection\u003csup\u003ee\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5(2.17)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.161\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eelevated blood glucose\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e12(5.22)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e3(2.08)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.178\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"4\"\u003eNote: The protein remission timepoints include the initial 6-month treatment period.\u003c/td\u003e\u003c/tr\u003e \u003ctr\u003e\u003ctd colspan=\"4\"\u003e\u003csup\u003ea\u003c/sup\u003e 3 months refers to the assessment conducted halfway through the treatment period.\u003c/td\u003e\u003c/tr\u003e \u003ctr\u003e\u003ctd colspan=\"4\"\u003e\u003csup\u003eb\u003c/sup\u003e 6 months refers to the assessment at the end of the treatment period\u003c/td\u003e\u003c/tr\u003e \u003ctr\u003e\u003ctd colspan=\"4\"\u003e\u003csup\u003ec\u003c/sup\u003e 12 months refer to follow-up assessments after treatment completion.\u003c/td\u003e\u003c/tr\u003e \u003ctr\u003e\u003ctd colspan=\"4\"\u003e\u003csup\u003ed\u003c/sup\u003e24 months refer to follow-up assessments after treatment completion.\u003c/td\u003e\u003c/tr\u003e \u003ctr\u003e\u003ctd colspan=\"4\"\u003e\u003csup\u003ee\u003c/sup\u003especial site infection including 2 cases of cellulitis, 2 case of pulmonary tuberculosis, and 1 case of purulent meningitis\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec12\" class=\"Section2\"\u003e \u003ch2\u003eEffect of glucocorticoid therapy on the prognosis of children with IgAN\u003c/h2\u003e \u003cp\u003eThe final follow-up was conducted on September 30, 2024. The median follow-up duration was 130.97 months (interquartile range: 101.58-168.65 months), during which a total of 28 endpoint events were recorded. In the GC\u0026thinsp;+\u0026thinsp;RASB group, 12 cases (5.22%) of IgAN endpoint events were observed, compared to 16 cases (11.11%) in the RASB group. This difference was statistically significant (P\u0026thinsp;=\u0026thinsp;0.035). Kaplan-Meier survival analysis revealed that the cumulative survival rates for IgAN patients in the GC\u0026thinsp;+\u0026thinsp;RASB group at 50, 100, 150, and 200 months were 99.1%, 98.6%, 96.6%, and 88.3%, respectively. In contrast, the corresponding cumulative kidney survival rates in the RASB group were 99.30%, 96.90%, 89.90%, and 70.50%, respectively. The difference in cumulative survival rates between the two groups was statistically significant (Log-rank test: χ\u0026sup2;=5.245, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.022, Fig. A). When stratified by eGFR levels, a significant difference in cumulative survival rates between the two groups was observed when eGFR was \u0026gt;\u0026thinsp;50 ml/min/1.73 m\u0026sup2; (Log-rank test: χ\u0026sup2;=5.120, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.024, Fig. B). However, no significant difference was noted when eGFR was \u0026le;\u0026thinsp;50 ml/min/1.73 m\u0026sup2; (Log-rank test: χ\u0026sup2;=0.017, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.897, Fig. C). In terms of 24h-UP levels, no significant difference in cumulative survival rates was found between the two groups when 24h-UP was \u0026lt;\u0026thinsp;1 g/d (Log-rank test: χ\u0026sup2;=0.065, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.798, Fig. D). However, significant differences were observed when 24h-UP was \u0026ge;\u0026thinsp;1 g/d and \u0026lt;\u0026thinsp;3 g/d (Log-rank test: χ\u0026sup2;=8.806, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.003,Fig. E) and when 24h-UP was \u0026ge;\u0026thinsp;3 g/d (Log-rank test: χ\u0026sup2;=5.038, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.025,Fig. F).Further analysis within the GC\u0026thinsp;+\u0026thinsp;RASB group showed that when eGFR was \u0026gt;\u0026thinsp;50 ml/min/1.73 m\u0026sup2; and 24h-UP was \u0026ge;\u0026thinsp;1 g/d, a significant difference in cumulative kidney survival was observed (Log-rank test: χ\u0026sup2;=4.046, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.044,Fig. G). Conversely, no significant difference was noted when eGFR was \u0026le;\u0026thinsp;50 ml/min/1.73 m\u0026sup2; and 24h-UP was \u0026lt;\u0026thinsp;1 g/d (Log-rank test: χ\u0026sup2;=0.364, \u003cem\u003eP\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.546, Fig. H).\u003c/p\u003e \u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eAt the outset of the study, individuals in the GC+RASB group presented with higher serum creatinine and lower plasma albumin levels than those in the RASB group. The increased serum creatinine suggests a decline in renal function. Meanwhile, the reduced plasma albumin may point to substantial proteinuria or compromised liver function. These observations underscore the greater renal impairment and potential nutritional deficits in the GC+RASB group at the outset of the study. In terms of pathological manifestations, there were no obvious differences between\u0026nbsp;two groups, which proved that the two groups were comparable. This finding is consistent with the results of The Validation Study of the Oxford Classification of IgA nephropathy (VALIGA)[23], which demonstrated that the MEST-C score was almost identical in both the conservative and intervention groups. Specifically, the percentages of M, E, S, Tand C were similar between the two groups, indicating that the pathological features were well-balanced. At the follow-up endpoint, a significant difference in the complete remission rate of proteinuria was noted between the two groups (86.09% in the GC+RASB group vs. 46.53% in the RASB group, \u003cem\u003eP\u003c/em\u003e\u0026lt;0.001). This result underscores the superior efficacy of GC combined with RASB in achieving proteinuria remission. Children who develop ESKD face a significantly reduced life expectancy, averaging 19 years after starting dialysis and around 40 years following kidney transplantation [24]. This stark reality may explain why pediatricians often prescribe steroids in addition to ACE inhibitors or ARBs, aiming to achieve complete remission of the disease[25]. Regarding adverse events, children in the GC+RASB group were more likely to develop central obesity compared to those in the RASB group. However, this effect resolved after discontinuation of GC therapy, demonstrating the relative safety of GC in pediatric IgAN patients.\u0026nbsp;A recent randomized controlled trial[26] in adults demonstrated that an enteric-coated, extended-release formulation of budesonide significantly reduced proteinuria and stabilized eGFR. This finding provides further evidence for the role of mucosal immunity in IgAN pathogenesis and suggests that targeted mucosal therapies may reduce the need for systemic immunosuppression. This approach represents a promising future direction for the treatment of IgAN.\u003c/p\u003e\n\u003cp\u003eThe 200-month cumulative kidney survival rate in the GC+RASB group was 88.3%, significantly higher than the 70.5% observed in the RASB group. This finding indicates that GC treatment can effectively delay disease progression in IgAN. Further stratified analysis revealed that GC therapy significantly reduced the risk of progression to ESRD in children with an initial eGFR \u0026gt; 50 ml/min/1.73 m\u0026sup2; and proteinuria \u0026ge;1 g/d. Conversely, for patients with an initial eGFR \u0026le; 50 ml/min/1.73m\u0026sup2; or proteinuria \u0026lt;1 g/d, GC therapy didn\u0026rsquo;t provide additional benefits in terms of kidney survival. Our study aligns with both the KDIGO guidelines[9] and the recent IPNA guidelines[27] for pediatric IgAN, which recommend combining GC with RASB for children with proteinuria \u0026gt;1 g/day. Our findings confirm the effectiveness of this combined therapy in reducing proteinuria and improving kidney outcomes.\u0026nbsp;Second, our study found no significant differences in MEST-C scores between the two groups. This suggests that kidney biopsy may not be necessary for deciding when or if to initiate GC therapy in IgAN patients. The MEST-C score, while useful for prognostic staging, didn\u0026rsquo;t predict the response to GC therapy in our cohort.\u0026nbsp;Third, the long follow-up period in our study, with all children followed for over 5 years and a median follow-up duration of over 10 years, provides robust data on kidney outcomes.\u0026nbsp;This extended follow-up period is crucial for accurately assessing the long-term effects of treatment and disease progression in pediatric IgAN patients. Nevertheless, several studies have indicated that immunosuppressive therapy can still be effective in individuals with advanced chronic kidney disease. \u0026nbsp;For example, Tesar et al.[23] found that GC reduced the risk of progression to ESKD in IgAN patients with an eGFR \u0026le;50 mL/min/1.73 m\u0026sup2;. Similarly, Stangou [28]and Pozzi[29] showed that GC improved proteinuria and delayed kidney function decline in patients with an eGFR \u0026lt;30 mL/min/1.73 m\u0026sup2;. The differences in outcomes may be due to the higher prevalence of IgAN and faster eGFR decline in East Asia (China), as well as the shorter follow-up periods in the Stangou and Pozzi studies compared to ours.\u003c/p\u003e\n\u003cp\u003eDue to the prolonged follow-up duration in this study, evaluating drug tapering or the total GC dose was impractical. Additionally, the selection of treatment regimens was not based on a strict, predefined single criterion. Instead, it was determined by clinicians after a comprehensive evaluation of each patient\u0026apos;s clinical characteristics and pathological manifestations. Given the single-center, observational, and retrospective nature of this study, it is challenging to completely eliminate residual confounding factors. Although we made every effort to control for known confounding factors in our analysis, we cannot completely rule out the potential impact of selection bias and residual confounding on the results. We have emphasized these limitations and suggest that future studies could further validate our findings through more rigorous study designs, such as prospective cohort studies or randomized controlled trials.\u003c/p\u003e\n\u003cp\u003eIn conclusion，this study found that GC therapy can delay disease progression in children with IgAN. However, the benefits of GC treatment were only evident in pediatric IgAN who had an initial eGFR ＞50 ml/min/1.73 m\u0026sup2; and proteinuria levels\u0026ge; 1 g/d. In contrast, for children with an initial eGFR＜50 ml/min/1.73 m\u0026sup2;, or with proteinuria＜1 g/d, adding GC therapy did not significantly improve cumulative kidney survival outcomes.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eData availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDeidentified individual participant’s data will not be made available.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe would like to thank everyone involved in data collection, including all the parents for their cooperation in this study.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis work was supported by funds from Shenzhen Science and Technology Program (No. JCYJ20220530145001002).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor information\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors and Affiliations\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDepartment of Pediatric Intensive Care Unit, The Seventh Affiliated Hospital，Sun Yat-sen University, 628 Zhenyuan Road, Guangming District, Shenzhen,518107,China\u003c/p\u003e\n\u003cp\u003eHeyan Wu, Lidan Zhang\u003c/p\u003e\n\u003cp\u003eDepartment of\u0026nbsp;Pediatrics, Jinling Hospital, 305 East Zhongshan Road, Nanjing\u0026nbsp;210002, Jiangsu\u0026nbsp;Province, China\u003c/p\u003e\n\u003cp\u003eZhengkun Xia\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCorresponding author\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eCorrespondence to\u0026nbsp;Zhengkun Xia and Lidan Zhang\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics declarations\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eMoriyama, T., Tanaka, K., Iwasaki, C., Oshima, Y., Ochi, A., Kataoka, H., Itabashi, M., Takei, T., Uchida, K., \u0026amp; Nitta, K. (2014). Prognosis in IgA nephropathy: 30-year analysis of 1,012 patients at a single center in Japan. PloS one, 9(3), e91756. https://doi.org/10.1371/journal.pone.0091756\u003c/li\u003e\n \u003cli\u003eWyatt, R. J., Kritchevsky, S. B., Woodford, S. Y., Miller, P. M., Roy, S., 3rd, Holland, N. H., Jackson, E., \u0026amp; Bishof, N. A. (1995). IgA nephropathy: long-term prognosis for pediatric patients. The Journal of pediatrics, 127(6), 913\u0026ndash;919. https://doi.org/10.1016/s0022-3476(95)70027-7\u003c/li\u003e\n \u003cli\u003eYata, N., Nakanishi, K., Shima, Y., Togawa, H., Obana, M., Sako, M., Nozu, K., Tanaka, R., Iijima, K., \u0026amp; Yoshikawa, N. (2008). Improved renal survival in Japanese children with IgA nephropathy. Pediatric nephrology (Berlin, Germany), 23(6), 905\u0026ndash;912. https://doi.org/10.1007/s00467-007-0726-5\u003c/li\u003e\n \u003cli\u003eSuzuki, H., Kiryluk, K., Novak, J., Moldoveanu, Z., Herr, A. B., Renfrow, M. B., Wyatt, R. J., Scolari, F., Mestecky, J., Gharavi, A. G., \u0026amp; Julian, B. A. (2011). The pathophysiology of IgA nephropathy. Journal of the American Society of Nephrology : JASN, 22(10), 1795\u0026ndash;1803. https://doi.org/10.1681/ASN.2011050464\u003c/li\u003e\n \u003cli\u003eBagchi, S., Mani, K., Swamy, A., Barwad, A., Singh, G., Bhowmik, D., \u0026amp; Agarwal, S. K. (2021). Supportive Management of IgA Nephropathy With Renin-Angiotensin Blockade, the AIIMS Primary IgA Nephropathy Cohort (APPROACH) Study. Kidney international reports, 6(6), 1661\u0026ndash;1668. https://doi.org/10.1016/j.ekir.2021.02.018\u003c/li\u003e\n \u003cli\u003eCoppo, R., Amore, A., Gianoglio, B., Cacace, G., Picciotto, G., Roccatello, D., Peruzzi, L., Piccoli, G., \u0026amp; De Filippi, P. G. (1993). Angiotensin II local hyperreactivity in the progression of IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation, 21(6), 593\u0026ndash;602. https://doi.org/10.1016/s0272-6386(12)80031-x\u003c/li\u003e\n \u003cli\u003eTanaka, S., Ninomiya, T., Katafuchi, R., Masutani, K., Nagata, M., Tsuchimoto, A., Hirakata, H., Kitazono, T., \u0026amp; Tsuruya, K. (2016). The effect of renin-angiotensin system blockade on the incidence of end-stage renal disease in IgA nephropathy. Clinical and experimental nephrology, 20(5), 689\u0026ndash;698. https://doi.org/10.1007/s10157-015-1195-y\u003c/li\u003e\n \u003cli\u003eTunnicliffe, D. J., Reid, S., Craig, J. C., Samuels, J. A., Molony, D. A., \u0026amp; Strippoli, G. F. (2024). Non-immunosuppressive treatment for IgA nephropathy. The Cochrane database of systematic reviews, 2(2), CD003962. https://doi.org/10.1002/14651858.CD003962.pub3\u003c/li\u003e\n \u003cli\u003eStevens, P. E., Levin, A., \u0026amp; Kidney Disease: Improving Global Outcomes Chronic Kidney Disease Guideline Development Work Group Members (2013). Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Annals of internal medicine, 158(11), 825\u0026ndash;830. https://doi.org/10.7326/0003-4819-158-11-201306040-00007\u003c/li\u003e\n \u003cli\u003eKobayashi, Y., Fujii, K., Hiki, Y., \u0026amp; Tateno, S. (1986). Steroid therapy in IgA nephropathy: a prospective pilot study in moderate proteinuric cases. The Quarterly journal of medicine, 61(234), 935\u0026ndash;943.\u003c/li\u003e\n \u003cli\u003eKobayashi, Y., Fujii, K., Hiki, Y., Tateno, S., Kurokawa, A., \u0026amp; Kamiyama, M. (1988). Steroid therapy in IgA nephropathy: a retrospective study in heavy proteinuric cases. Nephron, 48(1), 12\u0026ndash;17. https://doi.org/10.1159/000184861\u003c/li\u003e\n \u003cli\u003ePozzi, C., Bolasco, P. G., Fogazzi, G. B., Andrulli, S., Altieri, P., Ponticelli, C., \u0026amp; Locatelli, F. (1999). Corticosteroids in IgA nephropathy: a randomised controlled trial. Lancet (London, England), 353(9156), 883\u0026ndash;887. https://doi.org/10.1016/s0140-6736(98)03563-6\u003c/li\u003e\n \u003cli\u003eRauen, T., Eitner, F., Fitzner, C., Sommerer, C., Zeier, M., Otte, B., Panzer, U., Peters, H., Benck, U., Mertens, P. R., Kuhlmann, U., Witzke, O., Gross, O., Vielhauer, V., Mann, J. F., Hilgers, R. D., Floege, J., \u0026amp; STOP-IgAN Investigators (2015). Intensive Supportive Care plus Immunosuppression in IgA Nephropathy. The New England journal of medicine, 373(23), 2225\u0026ndash;2236. https://doi.org/10.1056/NEJMoa1415463\u003c/li\u003e\n \u003cli\u003eLv, J., Zhang, H., Wong, M. G., Jardine, M. J., Hladunewich, M., Jha, V., Monaghan, H., Zhao, M., Barbour, S., Reich, H., Cattran, D., Glassock, R., Levin, A., Wheeler, D., Woodward, M., Billot, L., Chan, T. M., Liu, Z. H., Johnson, D. W., Cass, A.,\u0026nbsp;\u0026hellip;\u0026nbsp;TESTING Study Group (2017). Effect of Oral Methylprednisolone on Clinical Outcomes in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA, 318(5), 432\u0026ndash;442. https://doi.org/10.1001/jama.2017.9362\u003c/li\u003e\n \u003cli\u003eCoppo, R., Lofaro, D., Camilla, R. R., Bellur, S., Cattran, D., Cook, H. T., Roberts, I. S., Peruzzi, L., Amore, A., Emma, F., Fuiano, L., Berg, U., Topaloglu, R., Bilginer, Y., Gesualdo, L., Polci, R., Mizerska-Wasiak, M., Caliskan, Y., Lundberg, S., Cancarini, G.,\u0026nbsp;\u0026hellip;\u0026nbsp;Honsova, E. (2017). Erratum to: Risk factors for progression in children and young adults with IgA nephropathy: an analysis of 261 cases from the VALIGA European cohort. Pediatric nephrology (Berlin, Germany), 32(1), 193\u0026ndash;194. https://doi.org/10.1007/s00467-016-3506-2\u003c/li\u003e\n \u003cli\u003eLv, J., Wong, M. G., Hladunewich, M. A., Jha, V., Hooi, L. S., Monaghan, H., Zhao, M., Barbour, S., Jardine, M. J., Reich, H. N., Cattran, D., Glassock, R., Levin, A., Wheeler, D. C., Woodward, M., Billot, L., Stepien, S., Rogers, K., Chan, T. M., Liu, Z. H.,\u0026nbsp;\u0026hellip;\u0026nbsp;TESTING Study Group (2022). Effect of Oral Methylprednisolone on Decline in Kidney Function or Kidney Failure in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA, 327(19), 1888\u0026ndash;1898. https://doi.org/10.1001/jama.2022.5368\u003c/li\u003e\n \u003cli\u003eSchwartz, G. J., Mu\u0026ntilde;oz, A., Schneider, M. F., Mak, R. H., Kaskel, F., Warady, B. A., \u0026amp; Furth, S. L. (2009). New equations to estimate GFR in children with CKD. Journal of the American Society of Nephrology : JASN, 20(3), 629\u0026ndash;637. https://doi.org/10.1681/ASN.2008030287\u003c/li\u003e\n \u003cli\u003eChi, X. H., Li, G. P., Wang, Q. S., Qi, Y. S., Huang, K., Zhang, Q., \u0026amp; Xue, Y. M. (2017). CKD-EPI creatinine-cystatin C glomerular filtration rate estimation equation seems more suitable for Chinese patients with chronic kidney disease than other equations. BMC nephrology, 18(1), 226. https://doi.org/10.1186/s12882-017-0637-z\u003c/li\u003e\n \u003cli\u003eKidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group (2021). KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney international, 100(4S), S1\u0026ndash;S276. https://doi.org/10.1016/j.kint.2021.05.021\u003c/li\u003e\n \u003cli\u003ede Simone, G., Mancusi, C., Hanssen, H., Genovesi, S., Lurbe, E., Parati, G., Sendzikaite, S., Valerio, G., Di Bonito, P., Di Salvo, G., Ferrini, M., Leeson, P., Moons, P., Weismann, C. G., \u0026amp; Williams, B. (2022). Hypertension in children and adolescents. European heart journal, 43(35), 3290\u0026ndash;3301. https://doi.org/10.1093/eurheartj/ehac328\u003c/li\u003e\n \u003cli\u003eTrimarchi, H., Barratt, J., Cattran, D. C., Cook, H. T., Coppo, R., Haas, M., Liu, Z. H., Roberts, I. S., Yuzawa, Y., Zhang, H., Feehally, J., IgAN Classification Working Group of the International IgA Nephropathy Network and the Renal Pathology Society, \u0026amp; Conference Participants (2017). Oxford Classification of IgA nephropathy 2016: an\u0026nbsp;update from the IgA Nephropathy Classification Working Group. Kidney international, 91(5), 1014\u0026ndash;1021. https://doi.org/10.1016/j.kint.2017.02.003\u003c/li\u003e\n \u003cli\u003eShima, Y., Nakanishi, K., Hama, T., Mukaiyama, H., Sato, M., Tanaka, Y., Tanaka, R., Kaito, H., Nozu, K., Sako, M., Iijima, K., \u0026amp; Yoshikawa, N. (2020). Crescentic IgA nephropathy in children. Pediatric nephrology (Berlin, Germany), 35(6), 1005\u0026ndash;1014. https://doi.org/10.1007/s00467-020-04483-w\u003c/li\u003e\n \u003cli\u003eTesar, V., Troyanov, S., Bellur, S., Verhave, J. C., Cook, H. T., Feehally, J., Roberts, I. S., Cattran, D., Coppo, R., \u0026amp; VALIGA study of the ERA-EDTA Immunonephrology Working Group (2015). Corticosteroids in IgA Nephropathy: A Retrospective Analysis from the VALIGA Study. \u003cem\u003eJournal of the American Society of Nephrology : JASN\u003c/em\u003e, \u003cem\u003e26\u003c/em\u003e(9), 2248\u0026ndash;2258. https://doi.org/10.1681/ASN.2014070697\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eMitsnefes, M. M., Laskin, B. L., Dahhou, M., Zhang, X., \u0026amp; Foster, B. J. (2013). Mortality risk among children initially treated with dialysis for end-stage kidney disease, 1990-2010. \u003cem\u003eJAMA\u003c/em\u003e, \u003cem\u003e309\u003c/em\u003e(18), 1921\u0026ndash;1929. https://doi.org/10.1001/jama.2013.4208\u003c/li\u003e\n \u003cli\u003eCambier, A., Boyer, O., Deschenes, G., Gleeson, J., Couderc, A., Hogan, J., \u0026amp; Robert, T. (2020). Steroid therapy in children with IgA nephropathy. \u003cem\u003ePediatric nephrology (Berlin, Germany)\u003c/em\u003e, \u003cem\u003e35\u003c/em\u003e(3), 359\u0026ndash;366. https://doi.org/10.1007/s00467-018-4189-7\u003c/li\u003e\n \u003cli\u003eFellstr\u0026ouml;m, B. C., Barratt, J., Cook, H., Coppo, R., Feehally, J., de Fijter, J. W., Floege, J., Hetzel, G., Jardine, A. G., Locatelli, F., Maes, B. D., Mercer, A., Ortiz, F., Praga, M., S\u0026oslash;rensen, S. S., Tesar, V., Del Vecchio, L., \u0026amp; NEFIGAN Trial Investigators (2017). Targeted-release budesonide versus placebo in patients with IgA nephropathy (NEFIGAN): a double-blind, randomised, placebo-controlled phase 2b trial. Lancet (London, England), 389(10084), 2117\u0026ndash;2127. https://doi.org/10.1016/S0140-6736(17)30550-0\u003c/li\u003e\n \u003cli\u003eVivarelli, M., Samuel, S., Coppo, R., Barratt, J., Bonilla-Felix, M., Haffner, D., Gibson, K., Haas, M., Abdel-Hafez, M. A., Adragna, M., Brogan, P., Kim, S., Liu, I., Liu, Z. H., Mantan, M., Shima, Y., Shimuzu, M., Shen, Q., Trimarchi, H., Hahn, D.,\u0026nbsp;\u0026hellip;\u0026nbsp;International Pediatric Nephrology Association (2025). IPNA clinical practice recommendations for the diagnosis and management of children with IgA nephropathy and IgA vasculitis nephritis. Pediatric nephrology (Berlin, Germany), 40(2), 533\u0026ndash;569. https://doi.org/10.1007/s00467-024-06502-6\u003c/li\u003e\n \u003cli\u003eStangou, M., Ekonomidou, D., Giamalis, P., Liakou, H., Tsiantoulas, A., Pantzaki, A., Papagianni, A., Efstratiadis, G., Alexopoulos, E., \u0026amp; Memmos, D. (2011). Steroids and azathioprine in the treatment of IgA nephropathy. Clinical and experimental nephrology, 15(3), 373\u0026ndash;380. https://doi.org/10.1007/s10157-011-0415-3\u003c/li\u003e\n \u003cli\u003ePozzi C. (2016). Treatment of IgA nephropathy. Journal of nephrology, 29(1), 21\u0026ndash;25. https://doi.org/10.1007/s40620-015-0248-3\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"pediatric-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"pnep","sideBox":"Learn more about [Pediatric Nephrology](http://link.springer.com/journal/467)","snPcode":"467","submissionUrl":"https://www.editorialmanager.com/pnep/default2.aspx","title":"Pediatric Nephrology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"IgA nephropathy, Glucocorticoids, Renin-angiotensin system blocker, Children, Kidney Outcomes","lastPublishedDoi":"10.21203/rs.3.rs-5996564/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5996564/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e: The efficacy of glucocorticoid (GC) in the management of immunoglobulin A nephropathy (IgAN) remains highly controversial. The study was conducted to analyze the efficacy and kidney outcomes of GC in the treatment of pediatric IgAN.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMethods:\u003c/strong\u003e Using the follow-up data of children with chronic kidney disease from the Department of Pediatrics at Jinling Hospital between January 2000 and December 2020, we selected children with primary IgAN who were ≤18 years old, confirmed by renal biopsy, and had undergone regular follow-up for more than 2 years. Patients who had previously used other immunosuppressive agents or had not received renin-angiotensin system blocker (RASB) treatment were excluded. The selected patients were divided into two groups based on their prior treatment regimens: the GC+RASB group and the RASB group. The primary outcome was a composite of a 40% decrease in estimated glomerular filtration rate (eGFR) from baseline, kidney failure, or death due to kidney disease.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults:\u003c/strong\u003e A total of 374 patients (149 females) were enrolled, with 230 in the GC+RASB group and 144 in the RASB group. At baseline, the GC+RASB group had lower albumin and higher creatinine levels (all \u003cem\u003eP\u003c/em\u003e \u0026lt; 0.05). From 6 months of treatment, the GC+RASB group showed higher urinary protein remission rates (\u003cem\u003eP\u003c/em\u003e\u0026lt; 0.05), but hematuria relief was similar between groups. Adverse events, including centripetal obesity, were more frequent in the GC+RASB group (\u003cem\u003eP\u003c/em\u003e= 0.001). After a median follow-up of 130.97 months, the GC+RASB group had fewer endpoint events (5.22% vs. 11.11%, \u003cem\u003eP\u003c/em\u003e = 0.035) and higher cumulative kidney survival rates, particularly in patients with eGFR \u0026gt;50 ml/min/1.73m² and 24h-UP ≥1 g/d (all \u003cem\u003eP\u003c/em\u003e \u0026lt; 0.05).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions:\u003c/strong\u003e GC therapy reduced the risk of progression to kidney failure in children with initial eGFR \u0026gt;50 ml/min/1.73 m² and proteinuria ≥1 g/d. No additional kidney survival benefit was observed in children with eGFR ≤50 ml/min/1.73 m² or proteinuria \u0026lt;1 g/d.\u003c/p\u003e","manuscriptTitle":"Retrospective Analysis of Glucocorticoid Therapy in Pediatric immunoglobulin A Nephropathy: Kidney Outcomes and Efficacy","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-04-28 11:27:58","doi":"10.21203/rs.3.rs-5996564/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"reviewerAgreed","content":"","date":"2025-04-23T06:48:06+00:00","index":0,"fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-04-20T16:36:40+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-04-20T16:10:25+00:00","index":"","fulltext":""},{"type":"submitted","content":"Pediatric Nephrology","date":"2025-04-19T13:04:14+00:00","index":"","fulltext":""},{"type":"decision","content":"Minor Revisions Needed","date":"2025-03-03T07:19:20+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"pediatric-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"pnep","sideBox":"Learn more about [Pediatric Nephrology](http://link.springer.com/journal/467)","snPcode":"467","submissionUrl":"https://www.editorialmanager.com/pnep/default2.aspx","title":"Pediatric Nephrology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"c3692d37-504f-4b4c-8cd8-540fdb52353c","owner":[],"postedDate":"April 28th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2025-07-21T16:03:59+00:00","versionOfRecord":{"articleIdentity":"rs-5996564","link":"https://doi.org/10.1007/s00467-025-06845-8","journal":{"identity":"pediatric-nephrology","isVorOnly":false,"title":"Pediatric Nephrology"},"publishedOn":"2025-07-15 15:57:32","publishedOnDateReadable":"July 15th, 2025"},"versionCreatedAt":"2025-04-28 11:27:58","video":"","vorDoi":"10.1007/s00467-025-06845-8","vorDoiUrl":"https://doi.org/10.1007/s00467-025-06845-8","workflowStages":[]},"version":"v1","identity":"rs-5996564","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-5996564","identity":"rs-5996564","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}