Renal Failure最新文献

{"title":"Domain-specific physical activity and sedentary behavior in relation to chronic kidney disease: a cross-sectional analysis of 24,950 U.S. adults in NHANES 1999-2012.","authors":"Nanhui Zhang, Jia Shi","doi":"10.1080/0886022X.2025.2525460","DOIUrl":"10.1080/0886022X.2025.2525460","url":null,"abstract":"<p><p>The independent and domain-specific associations between physical activity (PA) and chronic kidney disease (CKD) remain underexplored. This study investigates the relationships between leisure-time, occupational, and transportation-related PA, along with sedentary behavior, and CKD prevalence in a nationally representative U.S. adult cohort. We analyzed 24,950 participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2012. PA and sedentary behavior were assessed <i>via</i> validated questionnaires. Participants were classified based on adherence to physical activity guidelines (≥150 min/week). Multivariable logistic regression and restricted cubic splines were used to evaluate dose-response and non-linear associations. We found that meeting PA guidelines for total, leisure-time, and occupational PA was independently associated with lower odds of CKD (OR [95% CI]: 0.82 [0.73-0.93], 0.86 [0.76-0.97], and 0.85 [0.76-0.96], respectively). No significant association was observed for transportation-related PA. Sedentary behavior exceeding 6 h/day was associated with higher CKD prevalence. These associations were more pronounced in women, and dose-response patterns were evident across PA domains. This large-scale cross-sectional study identifies robust, domain-specific inverse associations between PA and CKD prevalence, particularly among women. Findings support stratified behavioral interventions targeting leisure and occupational activity domains, alongside sedentary behavior reduction, to mitigate CKD burden. Prospective studies are warranted to confirm causal pathways.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2525460"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144601317","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":"Development and validation of a nomogram for predicting calcification of arteriovenous access in hemodialysis patients.","authors":"Xueying Li, Xiaocui Wang, Bonan Yan, Yuanke Zhou, Ling Li, Xiaopeng Huang, Qiqi Wang, Enjie Tang","doi":"10.1080/0886022X.2025.2542980","DOIUrl":"10.1080/0886022X.2025.2542980","url":null,"abstract":"<p><strong>Background: </strong>In patients with end-stage renal disease (ESRD), vascular calcification significantly impairs hemodialysis (HD) vascular access functionality, compromising both dialysis efficacy and long-term patency. Early risk prediction of vascular calcification facilitates timely clinical interventions to preserve vascular access integrity.</p><p><strong>Methods: </strong>A cross-sectional analysis was performed. Risk factors for vascular calcification in CKD patients were identified from the literature and Kidney Disease: Improving Global Outcomes guidelines. All variable selection and model training procedures were conducted on the training set. Univariate logistic regression was performed for all candidate variables. A nomogram was then constructed based on the final multivariate logistic model to facilitate clinical interpretation.</p><p><strong>Result: </strong>A total of 136 HD patients were included. The predictive model, relying on arteriovenous (AV) access usage time, hip circumference, and diabetes status, is reliable and clinically actionable tool for predicting AV access calcification. Its robust performance across validation and subgroup analyses supports its potential for integration into routine clinical practice.</p><p><strong>Conclusion: </strong>This study developed a nomogram-based predictive model for calcification, providing a simple, cost-effective, and reliable tool for early risk assessment. Monitoring hip circumference may serve as a practical approach for identifying high-risk patients, allowing for timely intervention and improved vascular access outcomes.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2542980"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144837424","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":"Glycyrrhizin alleviates contrast-induced acute kidney injury via inhibiting HMGB1-mediated renal tubular epithelial cells ferroptosis.","authors":"Fang-Yuan Tian, Kun Liu, Zhi-Yao Tang, Ge Zhou, Guang-Liang Zhou, Rui-Feng Chen, Hao-Bo Liu, Wei-Jin Fang, Xiao-Cong Zuo, Ling-Yun Zhou","doi":"10.1080/0886022X.2025.2548613","DOIUrl":"10.1080/0886022X.2025.2548613","url":null,"abstract":"<p><p>Contrast-induced acute kidney injury (CI-AKI) is the third leading cause of AKI, but there are no effective preventive or therapeutic measures in clinical practice. Glycyrrhizin, a bioactive compound isolated from the <i>Glycyrrhiza glabra</i> L., exhibits anti-inflammatory effects; however, the effects and mechanisms of glycyrrhizin on CI-AKI remain unknown. In present study, the effects of glycyrrhizin on renal dysfunction and tissue damage were evaluated in CI-AKI rats and mice. And the mechanisms were further investigated in iohexol treated renal tubular epithelial cells. Molecular docking and network pharmacology were used to discover the binding targets of glycyrrhizin and identify potential pathogenic pathway. Gene knockout mice and gene silencing cells were used to detect whether glycyrrhizin alleviated CI-AKI through target proteins mediated pathway. Results showed that both pretreatment and co-treatment with glycyrrhizin could alleviate iohexol-induced renal dysfunction and pathological damage <i>in vivo</i>. Similarly, glycyrrhizin could improve iohexol-induced decrease in cell viability of both HK-2 cells and primary mice renal tubular epithelial cells. Mechanistically, glycyrrhizin could directly bind to the active site of HMGB1, then blocking iohexol-induced ferroptosis of renal tubular epithelial cells. HMGB1 silencing was able to inhibit overactivation of AMPK/Beclin-1 axis during CI-AKI, and iohexol-downregulated protein expressions of GPX4 and SLC7A11 were reversed in kidneys of AMPK knockout mice. Comparable results were obtained <i>in vitro</i> with AICAR treatment. Our study is the first to demonstrate that glycyrrhizin exerts both protective and therapeutic effect on CI-AKI by inhibiting tubular epithelial cell ferroptosis <i>via</i> HMGB1/AMPK/Beclin-1 axis, providing a potential choice for treating CI-AKI.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2548613"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12404086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966443","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":"Association of chaperone-mediated autophagy with the mechanisms of vascular calcification in diabetic nephropathy.","authors":"Yaling Zhang, Xianglong Meng, Ming Li","doi":"10.1080/0886022X.2025.2542530","DOIUrl":"10.1080/0886022X.2025.2542530","url":null,"abstract":"<p><p><b>Background:</b> Vascular calcification and autophagy play pivotal roles in the pathogenesis of diabetic nephropathy (DN), though the underlying molecular mechanisms remain unclear. <b>Methods:</b> Differential expression analysis and weighted gene co-expression network analysis were performed on the GSE30529 dataset to identify candidate genes associated with DN. Subsequently, Mendelian randomization analysis was utilized to isolate genes with a causal relationship to DN. DN biomarkers were further validated based on their expression profiles in both the GSE30529 training set and the GSE96804 validation set. Gene set enrichment analysis, immune infiltration analysis, drug prediction, and molecular regulatory network construction were then conducted. Reverse transcription-quantitative PCR (RT-qPCR) was used to assess the expression of biomarkers in clinical DN and normal samples. <b>Results:</b> A total of 286 candidate genes were identified in the GSE30529 dataset, of which seven were linked to DN progression. JCHAIN and IFI44L were highlighted as biomarkers due to their upregulated expression and their association with DN risk. These biomarkers were predominantly enriched in immune-related pathways and were strongly correlated with specific immune cell populations. Expression of <i>IFI44L</i> was found to be potentially regulated by miRNAs and the transcription factor YY1. Furthermore, potential DN therapeutic targets, including JCHAIN and IFI44L, were identified. RT-qPCR confirmed elevated expression levels of JCHAIN (<i>p</i> = 0.0155) and IFI44L (<i>p</i> = 0.0203) in DN samples, consistent with trends observed in the GSE30529 and GSE96804 datasets. <b>Conclusions:</b> The investigation identified VC-CMARGs <i>JCHAIN</i> and <i>IFI44L</i> as promising biomarkers, offering valuable insights for the clinical diagnosis and treatment of DN.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2542530"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789812","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":"Association between time-weighted average glucose concentration or glucose variability and acute kidney injury among coronary artery disease patients with prediabetes.","authors":"Jiaxin Ren, Ge Wang, Yizhe Zhou, Wei Gong, Hongjia Zhang, Yan Yan","doi":"10.1080/0886022X.2025.2549412","DOIUrl":"10.1080/0886022X.2025.2549412","url":null,"abstract":"<p><strong>Aims: </strong>To validate the effectiveness of intensive glycemic control in preventing acute kidney injury (AKI) among patients with coronary artery disease (CAD) and prediabetes.</p><p><strong>Methods: </strong>This investigation employed data from the Prospective Registry of the Current Status of Care for Patients with CAD database. Glycemic control was evaluated using the time-weighted average glucose (TWAG) and the glucose coefficient of variation (CV) for each participant. The primary outcome was AKI occurrence.</p><p><strong>Results: </strong>A total of 2,454 CAD patients with prediabetes were included between January 2022 and June 2023. The mean age was 62.6 ± 10.3 years, with 27.1% female. In univariate analysis, each 1 mmol/L increase in TWAG was associated with a 1.51-fold (95% confidence interval (CI): 1.36-1.68) higher incidence of AKI. After stepwise adjustment for covariates, the odds ratio (OR) remained significant at 1.50 (95% CI: 1.35-1.67). Similarly, glucose CV showed a positive correlation with AKI risk; a 0.1-unit increase in CV was linked to approximately a 44% higher risk. When both TWAG and CV were included simultaneously in the model, each maintained an independent positive association with AKI. Restricted cubic spline analyses revealed a dose-dependent increase in AKI risk with rising TWAG and CV. Subgroup analyses confirmed the positive relationship between TWAG, glucose variability, and AKI risk.</p><p><strong>Conclusions: </strong>Our study reveals an association between TWAG or CV of glucose and AKI in individuals with both CAD and prediabetes. These findings highlight the potential value of continuous glucose monitoring and managing glycemic variability to reduce AKI risk in this population.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2549412"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12409916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966373","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":"4-Methoxylonchocarpin protects against cisplatin induced acute kidney injury via regulating ferroptosis.","authors":"Nan Jiao, Baodong Wang, Qiong Zhang, Yuxiang Liu, Fen Zhao","doi":"10.1080/0886022X.2025.2545941","DOIUrl":"10.1080/0886022X.2025.2545941","url":null,"abstract":"<p><strong>Background: </strong>Traditional Chinese medicine active ingredients have been increasingly recognized for their pivotal role in the treatment of acute kidney injury (AKI).</p><p><strong>Methods: </strong>This study aimed to investigate the reno-protective effects and underlying mechanisms of 4-Methoxylonchocarpin (4ML), an extract from <i>Abrus precatorius Linne</i>, in a cisplatin-induced AKI model. Kidney injury was assessed through a comprehensive evaluation of renal function indicators and histopathological changes. The impact of 4ML on ferroptosis and AMPK pathways was examined by measuring lipid peroxidation biomarkers and iron ion following low and high dose 4ML treatments in mice. <i>In vitro</i> experiments, using HK-2 cells to assess ferroptosis biomarkers and cell proliferation with or without 4ML treatment, and in the presence of selective inhibitors or activators of ferroptosis and AMPK, to elucidate the potential mechanisms.</p><p><strong>Results: </strong>4ML administration significantly attenuated cisplatin-induced AKI in both mice models and HK-2 cells. Mechanistic studies revealed that 4ML treatment markedly reduced ferroptosis and activated the AMPK pathway, as evidenced by altered expression levels of GSH, GPX4, MDA, LPO, and iron ions. The activation of AMPK pathway by 4ML contributed to the amelioration of AKI. Conversely, the induction of ferroptosis and inhibition of AMPK attenuated the protective effects of 4ML.</p><p><strong>Conclusion: </strong>These findings suggest that 4ML as a promising therapeutic agent for cisplatin-induced AKI, primarily through inhibiting ferroptosis and regulating AMPK. This study provides further evidence supporting the potential of traditional Chinese medicine-derived compounds in the management of AKI.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2545941"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12344684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144837422","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":"Finerenone in non-diabetic CKD: an underexplored therapeutic opportunity.","authors":"Yu Zhao, Wenyun Wang, Jiaxing Nie, Jiaying Zhou, Zhilong Dong","doi":"10.1080/0886022X.2025.2559107","DOIUrl":"10.1080/0886022X.2025.2559107","url":null,"abstract":"","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2559107"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086963","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":"Collapse of dialysis services and preventable mortality in Ecuador: a national crisis in chronic kidney disease care with global implication.","authors":"Jorge Vasconez-Gonzalez, María de Lourdes Noboa-Lasso, Juan S Izquierdo-Condoy, Esteban Ortiz-Prado","doi":"10.1080/0886022X.2025.2561787","DOIUrl":"10.1080/0886022X.2025.2561787","url":null,"abstract":"","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2561787"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150664","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":"Assessment, molecular mechanisms and therapeutic targets for renal functional reserve.","authors":"Zhike Fu, Yueyi Deng","doi":"10.1080/0886022X.2025.2526686","DOIUrl":"10.1080/0886022X.2025.2526686","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) represents a significant global health challenge. Despite the availability of treatments, there remains a considerable residual risk of disease progression with current therapeutic approaches. Glomerular filtration rate (GFR) can increase due to various physiological and pathological stress responses, and the difference between the maximum GFR and the baseline GFR is termed renal functional reserve (RFR). A decline in RFR has been observed to occur well before CKD is clinically diagnosed. In addition, prolonged pathological stimulation of RFR may promote the development of other metabolic, hemodynamic, inflammatory, and fibrotic processes, which can ultimately drive CKD progression. This review consolidates the current evidence on the molecular mechanisms that underlie the initiation and decline of RFR, a phase that remains largely unaddressed as a primary treatment target but is gaining recognition for its critical role in CKD pathophysiology. Additionally, various methods for the safe and effective assessment of RFR are discussed. Recent clinical trial highlight promising new drug therapies and dietary strategies for the management of subclinical stages of CKD.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2526686"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12462421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145138513","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":"Evaluating gene variations in autosomal dominant polycystic kidney disease patients using whole exome sequencing and phenotype to genotype analysis.","authors":"Hande Aypek, Rumeysa Fatma Balaban, Nuseybe Huriyet, Ebrucan Bulut, Gulsah Cecener, Suat Akgur, Orhan Gorukmez, Ufuk Unal, Guven Ozkaya, Alparslan Ersoy, Aysegul Oruc, Cuma Bulent Gul, Abdulmecit Yildiz","doi":"10.1080/0886022X.2025.2547306","DOIUrl":"10.1080/0886022X.2025.2547306","url":null,"abstract":"<p><p>Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent hereditary kidney disorder. Between 85% and 90% of cases result from variations in the <i>PKD1</i> and <i>PKD2</i> genes. Over 30 genes have been associated with ADPKD, contributing to its heterogeneity. This study aimed to investigate novel variations in the <i>PKD1</i>, <i>PKD2,</i> and ADPKD-related genes through whole-exome sequencing (WES) and combine the genotype and phenotype data of the patients. WES was performed on peripheral blood samples from 44 ADPKD patients, and variations were evaluated and classified based on ACMG criteria. A heterozygous pathogenic/likely pathogenic (P/LP) <i>PKD1</i> variant was identified in 33 patients (75%). Seven patients had a heterozygous P/LP <i>PKD2</i> variant (15.9%). No heterozygous P/LP <i>PKD1</i> or <i>PKD2</i> variant was found in 4 patients (9.1%), and one of them (2.3%) had a heterozygous pathogenic <i>PKHD1</i> variant. Thirteen novel <i>PKD1</i> variations were identified, with nine associated with fast estimated glomerular filtration rate (eGFR) decline. Potentially pathogenic Variants of Uncertain Significance in <i>ALG9, CEP290, NPHP4</i>, <i>WDR19</i>, and <i>TTC21B</i> were identified in three patients lacking <i>PKD1/PKD2</i> variants. Survival analysis indicated that patients with <i>PKD1</i> or <i>PKD2</i> or without any <i>PKD1/PKD2</i> mutations experienced a similar age of onset for end-stage kidney disease. The annual decline in eGFR was significantly higher in patients with a <i>PKD1</i> mutation than in those with a <i>PKD2</i> mutation, along with a higher Mayo Class. Genetic studies evaluating novel variants in the <i>PKD1</i>, <i>PKD2</i>, and ADPKD-related genes alongside patients' clinical data are essential for a deeper understanding of ADPKD diagnosis, prognosis, and pathology.</p>","PeriodicalId":20839,"journal":{"name":"Renal Failure","volume":"47 1","pages":"2547306"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207331","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}