Renal Failure最新文献

{"title":"Joint impacts of air pollution and healthy lifestyles on kidney function decline: insights from a nationwide cohort study.","authors":"Leying Zhao, Cong Zhao, Zhen Wang, Zhenjie Chen, Huijuan Zheng, Sinan Ai, Jiayin Tao, Danting Li, Weiwei Sun, Yaoxian Wang","doi":"10.1080/0886022X.2025.2508295","DOIUrl":"10.1080/0886022X.2025.2508295","url":null,"abstract":"<p><p>Long-term exposure to ambient air pollution is a recognized environmental risk factor for chronic kidney disease (CKD), but its dynamic effects on kidney function remain incompletely understood. This nationwide longitudinal study included 5,306 participants from the China Health and Retirement Longitudinal Study (CHARLS) to examine associations between five major air pollutants (PM₁, PM_2.5, PM₁₀, NO₂, and O₃) and kidney function decline, measured by the annual slope of estimated glomerular filtration rate (eGFR). Air pollutant exposures were assessed both as continuous variables and dichotomized by median levels. Higher exposure to PM₁, PM_2.5, PM₁₀, and NO₂ was consistently associated with faster eGFR decline. In fully adjusted models, each 1 μg/m³ increase in PM_2.5 corresponded to a steeper decline in eGFR (<i>β</i> = -0.02; 95% CI: -0.03 to -0.02), while participants in high PM_2.5 areas had an annual decline of -0.51 mL/min/1.73 m² (95% CI: -0.72 to -0.31). O₃ showed a significant association only in binary models. Weighted quantile sum regression identified PM_2.5 and PM₁ as dominant contributors. A favorable lifestyle markedly mitigated pollution-related decline; under high PM₁ exposure, eGFR declined by -0.69 (95% CI: -1.06 to -0.33) in those with favorable lifestyles versus -2.20 (95% CI: -2.65 to -1.75) in those with unfavorable lifestyles. These findings were robust across multiple sensitivity analyses. These findings emphasize the adverse impact of long-term air pollution exposure on kidney function and suggest that healthy lifestyle behaviors may offer significant protective benefits.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2508295"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12123944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low sirtuin-1 levels are linked to erythropoietin resistance in hemodialysis patients.","authors":"Ebru Hekimgil, Cuma Bulent Gul","doi":"10.1080/0886022X.2025.2520909","DOIUrl":"10.1080/0886022X.2025.2520909","url":null,"abstract":"<p><strong>Introduction: </strong>Erythropoiesis-stimulating agents (ESAs) are widely used to manage anemia in chronic hemodialysis patients. However, some individuals exhibit ESA resistance, and its underlying mechanisms remain unclear. Sirtuin-1 (SIRT1), a key regulator of hypoxia and iron metabolism, may influence ESA responsiveness. This study investigates the relationship between SIRT1 levels and ESA resistance.</p><p><strong>Methods: </strong>This cross-sectional study analyzed 391 chronic hemodialysis patients, including ESA-treated and untreated individuals. ESA responsiveness was assessed using the Erythropoietin Resistance Index (ERI), calculated as weekly body-weight-adjusted ESA dose divided by hemoglobin concentration. Associations between SIRT1 levels, ERI quartiles, and ESA responsiveness were examined.</p><p><strong>Results: </strong>A total of 385 patients were included in the analysis. Serum SIRT1 levels were significantly lower in ESA-treated patients than in untreated individuals. A negative correlation was found between SIRT1 levels and ERI (r = -0.179, <i>p</i> < 0.001). Multiple regression analysis confirmed that both ERI (β = -0.158, <i>p</i> = 0.002) and ferritin levels (β = -0.121, <i>p</i> = 0.015) were independent negative predictors of SIRT1 (R²= 0.081). Patients with high ERI (≥50th percentile) had significantly lower SIRT1 levels. Logistic regression indicated that only SIRT1 was significantly associated with high ERI (B = -0.035, <i>p</i> = 0.018).</p><p><strong>Conclusion: </strong>This study examined the relationship between SIRT1 levels and ESA hyporesponsiveness in patients undergoing hemodialysis. The findings demonstrate that lower SIRT1 levels are associated with higher ERI values, suggesting a potential role for SIRT1 in modulating ESA resistance.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2520909"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary and plasma donor-derived cell-free DNA for noninvasive monitoring of BK polyomavirus-associated nephropathy in kidney transplant recipients: a prospective cohort study.","authors":"Luying Guo, Sulin Luo, Rongfang Shen, Pengpeng Yan, Meifang Wang, Tianlu Zhang, Junhao Lv, Guangjun Liu, Hongfeng Huang, Zhimin Chen, Huiping Wang, Wenhan Peng, Jianyong Wu, Jianghua Chen, Rending Wang","doi":"10.1080/0886022X.2025.2521452","DOIUrl":"https://doi.org/10.1080/0886022X.2025.2521452","url":null,"abstract":"<p><strong>Background: </strong>BK polyomavirus-associated nephropathy (BKPyVAN) is a major cause of allograft injury and dysfunction in kidney transplant recipients. Current monitoring tools, including viremia and biopsy, have limitations in sensitivity, invasiveness, and timing.</p><p><strong>Objective: </strong>To evaluate donor-derived cell-free DNA (dd-cfDNA) in urine and plasma as a dynamic, noninvasive biomarker for monitoring treatment response and predicting rejection risk in patients with biopsy-proven BKPyVAN.</p><p><strong>Methods: </strong>In this prospective cohort study, 25 kidney transplant recipients with biopsy-proved BKPyVAN were enrolled and stratified into two cohorts: conventional immunosuppression reduction (CISR, <i>n</i> = 20) and early immunosuppression reduction (EISR, <i>n</i> = 5). A total of 224 urine and plasma samples were collected before biopsy and at 1, 2, 3, and 6 months post-biopsy. dd-cfDNA levels were quantified and correlated with histological features and clinical outcomes.</p><p><strong>Results: </strong>Urinary dd-cfDNA levels significantly declined in the CISR cohort by month 2 (<i>p</i> < 0.01), preceding changes in creatinine and BKPyV reads. In the EISR cohort, urinary dd-cfDNA levels remained stable, suggesting early therapeutic response. Plasma dd-cfDNA effectively identified acute rejection, with elevations in two CISR patients. Histologic injury patterns, including edema and cast formation, correlated with urinary dd-cfDNA concentrations (<i>r</i> = 0.44-0.51, <i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>Combined urinary and plasma dd-cfDNA measurements are promising for noninvasive, dynamic surveillance of BKPyVAN and rejection risk in kidney transplant recipients. Larger, multicenter studies are warranted to define clinical thresholds and standardize integration into immunosuppression management.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2521452"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urotensin II system contributes to ischemic acute kidney injury in neonatal pigs.","authors":"Julia E de la Cruz, Olugbenga S Michael, Praghalathan Kanthakumar, Olufunke O Falayi, Samson A Iwhiwhu, Jeremiah M Afolabi, Ravi Kumar, Hitesh Soni, Adebowale Adebiyi","doi":"10.1080/0886022X.2025.2534018","DOIUrl":"10.1080/0886022X.2025.2534018","url":null,"abstract":"<p><p>The urotensin II (UII) system comprises UII, UII-related peptide (URP), and their shared receptor UT. Bioactive UII can be generated from its precursor, prepro-UII, through proteolytic cleavage by the serine protease furin. The kidney serves as a significant source of UII, with elevated levels reported in infants with chronic kidney disease. Here, we investigated the contribution of the UII system to the loss of kidney function during ischemia-reperfusion (IR)-induced acute kidney injury (AKI) in neonatal pigs. Intra-arterial renal infusion of porcine UII reduced renal blood flow and increased vascular resistance, effects reversed by the UT antagonist urantide. Although IR did not alter whole-kidney UT expression, it increased furin, UII, URP, and vascular UT levels. Urantide attenuated IR-induced kidney hypoperfusion, elevations in AKI biomarkers and circulating cytokines, and histological kidney injury. In primary neonatal pig proximal tubule epithelial cells (PTECs), chemical IR (cIR), modeled by 1 h of ischemia (ATP-, glucose-, and serum-depleted medium) followed by reperfusion (restoration of complete medium), elevated furin and UII production. The furin inhibitor SSM 3 trifluoroacetate (SSM 3) suppressed cIR-induced UII synthesis. Moreover, both urantide and SSM 3 mitigated cIR-induced PTEC injury. These findings suggest that in neonatal pigs: (1) renal IR upregulates furin, UII, and URP in kidney tissue and UT in the microvasculature, (2) furin promotes UII biosynthesis in renal epithelial cells, and (3) UT inhibition protects against ischemic AKI.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2534018"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preoperative systemic immune-inflammation index as a predictor of contrast-induced acute kidney injury in coronary artery disease: a multicenter cohort study.","authors":"Jinlong Zhu, Pei Yu, Xiaoying Zhang, Xiaoming Li, Jiaming Huang, Shumin Zhao, Qingyan Ruan, Yibo He, Yang Zhou, Kunming Bao, Jiaming Xiu, Lin Deng, Yunchen Liu, Yong Liu, Shiqun Chen, Kaihong Chen, Liling Chen","doi":"10.1080/0886022X.2025.2474204","DOIUrl":"10.1080/0886022X.2025.2474204","url":null,"abstract":"<p><strong>Background: </strong>Inflammation is a key contributor to contrast-induced acute kidney injury (CI-AKI), yet its predictive role remains unclear. The systemic immune-inflammation index (SII) is a novel inflammatory biomarker, but its association with CI-AKI risk in coronary artery disease (CAD) patients undergoing coronary angiography is not well established. This study aimed to evaluate the relationship between preoperative SII and CI-AKI in a large multicenter cohort.</p><p><strong>Methods: </strong>This retrospective cohort study analyzed CAD patients from five tertiary hospitals in China (2007-2020). Patients were stratified into SII tertiles, and multivariable logistic regression, restricted cubic splines (RCS), and two-piecewise logistic regression models were employed to assess the association between SII and CI-AKI risk.</p><p><strong>Results: </strong>Among 30,822 patients, 3,246 (10.5%) developed CI-AKI. Higher preoperative SII levels were associated with increased CI-AKI risk ([SII-M vs. SII-L]: OR = 1.22, 95% CI [1.09-1.36], <i>p</i> = 0.001; [SII-H vs. SII-L]: OR = 1.70, 95% CI [1.53-1.90], <i>p</i> < 0.001). RCS analysis demonstrated a nonlinear relationship (p for nonlinearity = 0.008). The inflection point was at 19.12 × 10¹¹/L. Below this inflection point, each 100-unit increase in SII correlated with a 5% higher CI-AKI risk (OR = 1.05, 95% CI [1.04-1.06], <i>p</i> < 0.001), while no significant association was observed above this level.</p><p><strong>Conclusion: </strong>Preoperative SII may be an independent predictor of CI-AKI risk in CAD patients undergoing undergoing coronary angiography, demonstrating a nonlinear dose-response relationship with a significant threshold effect. These findings suggest that SII may serve as a useful biomarker for early CI-AKI risk stratification in clinical practice.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2474204"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143693160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial DNA copy number as a genetic determinant of renal function: insights from bidirectional Mendelian randomization.","authors":"Suwei Wang, Yuanjing Yang, Zeyu Pang, Yidan Li, Ke Li, Yan Sun, Jurong Yang","doi":"10.1080/0886022X.2025.2542522","DOIUrl":"10.1080/0886022X.2025.2542522","url":null,"abstract":"<p><p><b>Background:</b> Observational studies suggest a correlation between mitochondrial DNA copy number (mtDNA-CN) and renal function; however, the causality remains uncertain. This study employed a two-sample bidirectional Mendelian randomization (MR) analysis to investigate the genetic causal relationship between mtDNA-CN and renal function. <b>Methods:</b> Genome-wide association study (GWAS) data for mtDNA-CN were obtained from the UK Biobank (<i>n</i> = 395,718), with renal function data primarily sourced from the CKDGen consortium and FinnGen studies. Four MR methods were employed, using inverse variance weighting as the primary approach, complemented by weighted median, MR Egger, and MR-PRESSO for sensitivity analyses. Multivariable MR (MVMR) assessed result robustness. Reverse MR treated renal function as the exposure. Validation was performed using additional mtDNA-CN GWAS data from the CHARGE UK Biobank (<i>n</i> = 465,809). <b>Results:</b> Forward MR analysis demonstrated a positive association between genetically predicted mtDNA-CN and estimated glomerular filtration rate (eGFR) [odds ratio (OR) = 1.007, 95% CI 1.003-1.012, <i>p</i> = 0.003]. MVMR suggested weaker evidence after adjusting for neutrophil count. Reverse MR revealed causal associations of urinary albumin-creatinine ratio (OR = 0.958, 0.923-0.994, <i>p</i> = 0.023) and microalbuminuria (OR = 0.981, 0.965-0.997, <i>p</i> = 0.021) with mtDNA-CN, though these effects were non-significant after multiple testing correction. Sensitivity and validation analyses confirmed robust. The findings from validation analyses were consistent. <b>Conclusion:</b> Our study suggests a potential causal association between mtDNA-CN and eGFR. However, the impact of confounding factors and the absence of consistent associations with other renal function markers underscore the necessity for further research to clarify the role of mtDNA-CN in renal function.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2542522"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transient decline and early recovery of noninvasive myocardial work after kidney transplantation: a prospective study.","authors":"Yulin Huang, Lin Jin, Xinyan Qiu, Canying Yang, Luyi Ping, Zhengyao Jiang, Hua Zou, Zhihong Zhang, Jiwei Wang","doi":"10.1080/0886022X.2025.2543930","DOIUrl":"10.1080/0886022X.2025.2543930","url":null,"abstract":"<p><strong>Background: </strong>Patients with chronic kidney disease (CKD) are at a high risk of cardiovascular disease. This study aims to observe the short-term changes of left ventricular (LV) myocardial work in stage 5 CKD patients with successful kidney transplantation (KT).</p><p><strong>Methods: </strong>45 stage 5 CKD patients who are candidates for KT were enrolled. Changes in clinical variables, laboratory data, routine transthoracic echocardiography, and noninvasive myocardial work (NIMW) were analyzed at pre-KT, 10 days, and 3 months post-KT. NIMW parameters include global myocardial work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE).</p><p><strong>Results: </strong>1) Renal function indicators, including blood urea nitrogen, serum creatinine, and estimated glomerular filtration rate improved significantly at 10 days post-KT. At 3 months post-KT, there appears to be a continuing recovery trend; 2) GWE, GWI, and GCW were significantly increased at 3 months post-KT, but GCW and GWI with an early decrease at 10 days post-KT; 3) At the 10 days post-KT, the changes in systolic blood pressure and hemoglobin were positively correlated with the changes in GWI. Meanwhile, the change in systolic blood pressure was also positively correlated with the change in GCW. The change in diastolic blood pressure was positively correlated with the change in GWW.</p><p><strong>Conclusion: </strong>LV systolic function doesn't improve in parallel with renal function after a successful KT. Steadily controlling blood pressure and correcting anemia is associated with improving myocardial work after KT, especially in the early post-transplant period.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2543930"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network pharmacology-based strategy to investigate pharmacological mechanisms of polysaccharide-free <i>Lycium barbarum</i> extract for chronic kidney disease treatment and verification in an animal model.","authors":"Meiyou Liu, Kai Gao, Jia Cui, Xiaoxiao Wu, Likun Ding, Tingting Fan, Juanli Zhang, Di Zhang, Danjun Ren, Aidong Wen, Jingwen Wang","doi":"10.1080/0886022X.2025.2539942","DOIUrl":"10.1080/0886022X.2025.2539942","url":null,"abstract":"<p><p><i>Lycium barbarum polysaccharides</i> (LBP) have shown renal protection effects. However, research on other active components of <i>L. barbarum</i> extract (ELB) for the therapy of chronic kidney disease (CKD) is limited. This study aims to investigate the renoprotective effects and molecular mechanisms of ELB in CKD. ELB was extracted from <i>L. barbarum</i> fruits using 85% ethanol reflux, followed by vacuum concentration and sequential extraction to remove polysaccharides. Chemical components and target genes were identified using TCMSP and UniProt databases, followed by pharmacology network construction and GO/KEGG pathway analysis. A 5/6 nephrectomy model in Sprague-Dawley rats was used to study the renoprotective effects of ELB, with H&E staining and biochemical analyses. Western blot analysis assessed IL-6 and VEGF expression in renal tissues. Chemical analysis of ELB identified 188 components, with 45 meeting screening criteria, and 34 linked to 94 target genes. The intersection with CKD-related genes yielded 39 overlapping genes, with quercetin having the most targets. GO/KEGG pathway analyses highlighted significant biological processes and pathways. A PPI network identified IL-6, VEGFA, CASP3, EGFR, ESR1, and PPARG as hub genes. In a 5/6 nephrectomy rat model, ELB treatment significantly reduced renal damage, serum BUN and SCr levels, as well as IL-6 and VEGF expression in renal tissues, validating its renoprotective effects and supporting bioinformatics predictions. This work identified the intricate components and pharmacological actions of ELB, which is devoid of LBP. The findings preliminarily confirm the potential of ELB as a novel therapeutic agent for preventing and managing CKD.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2539942"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12315129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144761126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalin alleviates sepsis-associated acute kidney injury through activation of the PPAR-γ/UCP1 signaling pathway.","authors":"Neng Bao, Ming-Jia Gu, Qiu-Ya Huang, Hai-Jian Sun, Xue-Xue Zhu, Xin Gu, Jin Wang, Xiang Yu, Qing-Bo Lu, Ya-Fen Yu","doi":"10.1080/0886022X.2025.2508908","DOIUrl":"10.1080/0886022X.2025.2508908","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to investigate the protective effect of baicalin on sepsis-associated acute kidney injury (SA-AKI) and its molecular mechanism.</p><p><strong>Materials and methods: </strong>An SA-AKI mouse model was established <i>via</i> lipopolysaccharide (LPS) injection. Baicalin's effects on renal function, oxidative stress, and apoptosis were evaluated using histopathology, dihydroethidium, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Bioinformatics, molecular docking, ribonucleic acid (RNA) sequencing, and Western blotting were employed to investigate the role of baicalin in regulating the peroxisome proliferator‑activated receptor‑γ (PPAR-γ)/uncoupling protein 1 (UCP1) pathway. Human kidney-2 cells were used for <i>in vitro</i> validation.</p><p><strong>Results: </strong>In this study, baicalin significantly ameliorated LPS-induced acute kidney injury by modulating the PPAR-γ/UCP1 signaling pathway. Both <i>in vivo</i> and <i>in vitro</i> experiments revealed that baicalin attenuates inflammation, oxidative stress, and apoptosis while restoring mitochondrial function. RNA sequencing analysis revealed significant upregulation of PPAR-γ/UCP1 in the baicalin-treated group. Further molecular docking and molecular dynamics simulations confirmed a stable interaction between baicalin and UCP1. Validation <i>via</i> small interfering RNA-mediated knockdown of PPAR-γ and UCP1 revealed that inhibition of the PPAR-γ/UCP1 pathway abrogated baicalin's protective effects, highlighting the critical role of this pathway in mediating baicalin's renoprotection.</p><p><strong>Conclusion: </strong>Baicalin protects against SA-AKI by activating the PPAR-γ/UCP1 signaling pathway. This study provides new insights into the mechanisms through which baicalin mitigates kidney injury in sepsis, suggesting its potential as a therapeutic agent for SA-AKI.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2508908"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12168399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144286422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Critical appraisal of systematic reviews and meta-analyses: a step-by-step guide for nephrologists.","authors":"Wisit Cheungpasitporn, Wannasit Wathanavasin, Charat Thongprayoon, Wisit Kaewput, Mihály Tapolyai, Tibor Fülöp","doi":"10.1080/0886022X.2025.2476736","DOIUrl":"10.1080/0886022X.2025.2476736","url":null,"abstract":"<p><strong>Background: </strong>Systematic reviews and meta-analyses play a pivotal role in evidence-based medicine, including nephrology, by consolidating findings from multiple studies. To maximize their utility, rigorous quality assessment during peer review is essential. Challenges such as heterogeneity, bias, and methodological flaws often undermine these studies, necessitating a structured appraisal process.</p><p><strong>Methods: </strong>This guide outlines a framework for nephrologists on appraising systematic reviews and meta-analyses. Key areas include heterogeneity assessment using the I² statistic, interpretation of forest plots for pooled effect estimates, and the use of funnel plots with Egger's test to identify potential publication bias. Risk of bias is evaluated using RoB 2 for randomized controlled trials and ROBINS-I for non-randomized studies. Subgroup and sensitivity analyses, along with meta-regression, address heterogeneity and examine the robustness of findings.</p><p><strong>Results: </strong>The I² statistic quantifies heterogeneity by estimating the proportion of variability in a meta-analysis. Funnel plots and Egger's test help detect publication bias. Major biases, such as selection, performance, detection, and publication bias, are identified using structured tools like AMSTAR 2, Cochrane RoB 2, and ROBINS-I. The GRADE framework further assesses the overall certainty of the evidence. Emphasis is placed on PRISMA compliance, protocol pre-registration, and transparent reporting of statistical analyses, subgroup, and sensitivity assessments. The inclusion of grey literature remains optional.</p><p><strong>Conclusion: </strong>By focusing on key areas such as heterogeneity, risk of bias, and robust statistical methods, this guide enables nephrologists to critically appraise systematic reviews and meta-analyses, fostering better clinical decision-making and improved patient care in nephrology.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2476736"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}