Kidney & blood pressure research最新文献

{"title":"Endothelial MicroRNA-214 Confers Angiotensin II Hypertension by Targeting eNOS in mice.","authors":"Shuzhen Li, Bing Liu, Shuang Kang, Bingyu Yang, Yue Zhang, Songming Huang, Aihua Zhang, Zhanjun Jia","doi":"10.1159/000546674","DOIUrl":"https://doi.org/10.1159/000546674","url":null,"abstract":"<p><p>MicroRNAs have been increasingly recognized for their roles in cardiovascular diseases. Among these microRNAs, miR-214 was reported to be involved in hypertension. However, the role of endothelial miR-214 in hypertension is still unknown. The aim of this study was to determine the role of cell-specific miR-214 on regulating blood pressure, as well as the potential mechanisms. miR-214 levels in hypertensive mice and cultured mouse aortic endothelial cells (MAECs) were detected and its role in Ang II-induced hypertension was examined. In mice and MAECs, Ang II significantly enhanced miR-214 levels, and anti-miR-214 markedly attenuated Ang II hypertension in line with enhanced eNOS/p-eNOS in aorta. Then we generated vascular endothelial cell-specific miR-214 knockout mice and found an anti-hypertensive phenotype in endothelial miR-214 conditional knock-out mice after Ang II treatment. In normotensive animals and MAECs, exogenous miR-214 administration reduced eNOS expression at protein and mRNA levels, in contrast, anti-miR-214 played an opposite role in regulating eNOS. By luciferase assay, our results confirmed that eNOS was a direct target gene for miR-214 in endothelial cells. However, smooth muscle cell-specific or renal tubular cell-specific deletion of miR-214 did not alter Ang II-induced hypertension. Thus, our findings suggested that endothelial miR-214 promoted Ang II hypertension by targeting eNOS in mice, which increased the understanding on the pathogenic mechanism of hypertension.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-21"},"PeriodicalIF":2.3,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydronephrosis-Associated Renal Fibrosis: Clinical Validation of Spp1 as a Biomarker and Therapeutic Target.","authors":"Xiao Wang, Jie-Hao Zhou, Guang Chen, Ji-Dong Chen, Hui Li, Wei-Min Shan, Wei-Xiao Li","doi":"10.1159/000546465","DOIUrl":"https://doi.org/10.1159/000546465","url":null,"abstract":"<p><strong>Background: </strong>Renal fibrosis is a key driver of chronic kidney disease (CKD), often leading to end-stage renal disease (ESRD). Secreted Phosphoprotein 1 (Spp1) is implicated in fibrotic processes, but its specific role in renal fibrosis, particularly associated with hydronephrosis, remains underexplored. This study investigates Spp1's involvement using transcriptomic analysis, machine learning, and clinical data integration.</p><p><strong>Methods: </strong>Renal tissues from sham-operated and UUO7 (unilateral ureteral obstruction) mice were analyzed via transcriptome sequencing to identify differentially expressed genes (DEGs). Hub genes were identified through Weighted Gene Co-expression Network Analysis (WGCNA) and pathway enrichment. LASSO regression pinpointed potential biomarkers, with Spp1 validated in mouse and human samples through RT-PCR and immunohistochemistry. Clinical correlations were drawn from hydronephrosis patient data.</p><p><strong>Results: </strong>Transcriptomic analysis revealed 5,219 DEGs, highlighting key pathways including IL-17, TNF, and PI3K/AKT. Spp1 emerged as a significant biomarker, strongly associated with tubular injury and fibrosis markers such as neutrophil gelatinase-associated lipocalin (NGAL). Logistic regression and ROC analyses confirmed Spp1 and urinary transferrin (U-TRF) as predictors of severe hydronephrosis, with high diagnostic accuracy (AUC: 0.898 for Spp1; 0.938 for U-TRF).</p><p><strong>Conclusions: </strong>Spp1 is a critical mediator in renal fibrosis and a promising biomarker for assessing hydronephrosis severity. Its diagnostic value, particularly when combined with U-TRF, underscores the need for further research into Spp1-targeted therapies in renal fibrosis.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-26"},"PeriodicalIF":2.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CFHR5 nephropathy case report: a novel variant characterized by tubulointerstitial kidney disease.","authors":"Rita Santarsiere, Giulia Florio, Annalisa Gonnella, Pierluigi D'Angiò, Simona Laurino, Miriam Zacchia, Francesca Del Vecchio Blanco, Alessandra F Perna, Francesco Trepiccione, Giuseppe Gigliotti","doi":"10.1159/000546321","DOIUrl":"https://doi.org/10.1159/000546321","url":null,"abstract":"<p><p>CFHR5 nephropathy is considered a subtype of C3 glomerulopathy. It was originally described in Greek Cypriot families and it is characterized by the time with the development of microscopic hematuria and proteinuria associated with a fast progression towards ESKD especially in men. These symptoms present an autosomal dominant inheritance pattern and are associated with the exon 2 to 3 duplication of the CFHR5 gene. Here, we describe a novel clinical phenotype associated with a variant of the CFHR5. The affected subjects present the clinical features of Autosomal Dominant Tubulo-interstitial Kidney Disease. They present with CKD of unknown origin with no hematuria nor proteinuria. Like the classical CFHR5 nephropathy, males have a worse prognosis than females, with a fast progression towards ESKD in the second-third decade of life. Kidney pathology shows severe tubular atrophy and interstitial fibrosis and infiltrate. Arteries involvement is characterized by thickening of the intima layer, while no major alterations are described at the glomerular level. Electron Microscopy confirms no interstitial or glomerular filtration barrier alterations.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-10"},"PeriodicalIF":2.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rethinking models of CKD care: a narrative review.","authors":"Hannah Wallace, J Oliver Daly, Min Jun, Craig Nelson","doi":"10.1159/000546562","DOIUrl":"https://doi.org/10.1159/000546562","url":null,"abstract":"<p><strong>Background: </strong>Chronic kidney disease (CKD) affects over 850 million people worldwide and is associated with significant morbidity and mortality. There has been recent expansion in treatment options to reduce CKD progression and cardiovascular risk, and it is essential that this translates into clinical practice.</p><p><strong>Summary: </strong>The primary objectives of this review were to outline current CKD care models and associated care gaps, and review the literature for alternative care models, with a focus on the early detection and management of CKD. Several care models have been proposed to improve CKD management including nurse-led, pharmacy-led, integrated care models and digital interventions, with mixed results.</p><p><strong>Key messages: </strong>There is a need for ongoing health systems and implementation research to improve translation of evidence into practice in the management of chronic kidney disease.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-17"},"PeriodicalIF":2.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension in living kidney donors has no effect on complement activation and fibrosis.","authors":"Nadine Wagner, Miriam Angeloni, Fulvia Ferrazzi, Janina Müller-Deile, Maike Büttner-Herold, Kerstin Amann, Christoph Daniel, Eva Vonbrunn","doi":"10.1159/000545750","DOIUrl":"https://doi.org/10.1159/000545750","url":null,"abstract":"<p><strong>Background: </strong>In the past, elevated blood pressure was considered an exclusion criterion for living kidney donation because of concerns about premature kidney failure. Hypertension leads to complement deposits and renal fibrosis in the kidney. Therefore, the aim of this study was to investigate whether increased complement deposits and fibrosis can be observed in grafts of hypertensive compared to normotensive living donors.</p><p><strong>Methods: </strong>Zero-time renal biopsies from 238 living donors (52 hypertensive) and the corresponding one-year protocol biopsies were examined for complement deposits of C1q, C3c, and MASP-2. Findings were compared to kidney biopsies from patients with hypertensive nephropathy. Further, renal fibrosis was visualized by Sirius Red staining, scored semiquantitatively and compared to biopsies from deceased donors and kidneys with hypertensive nephropathy. Additionally, zero-time biopsies from hypertensive (n = 6) and normotensive (n = 5) living donors were analyzed for expression of fibrosis-associated genes by multiplex mRNA analysis and compared to zero-time biopsies (n = 6) from deceased donors.</p><p><strong>Results: </strong>In all zero-time biopsies from living donors, complement deposits were minimal for C1q, C3c, and MASP-2 compared to samples with hypertensive nephropathy, regardless of whether the donor was hypertensive or normotensive. In one-year protocol biopsies, complement deposits were unchanged, while renal fibrosis was slightly but not significantly increased in hypertensive compared to normotensive living donors. Gene expression data showed that the 11 zero-time biopsies from hypertensive and normotensive living donors clustered together, and were clearly separated from the deceased donor biopsies.</p><p><strong>Conclusion: </strong>The use of kidneys from hypertensive living donors appears to have no or little effect on renal complement deposits and fibrosis one year after transplantation.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-21"},"PeriodicalIF":2.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Interdialytic Intervals on Sudden Cardiac Death in Chronic Kidney Disease Stage 5D Patients on a Twice-Weekly HD Schedule.","authors":"Prasanna Kumar, Kshama Savant, Athira Balakrishnan, Sreedharan Nair, Ravindra Prabhu Attur","doi":"10.1159/000546184","DOIUrl":"https://doi.org/10.1159/000546184","url":null,"abstract":"<p><strong>Background: </strong>End-stage kidney disease patients on maintenance haemodialysis (HD) are prone to increase cardiovascular and non-cardiovascular mortality in long and short interdialytic intervals of an intermittent thrice-weekly schedule. Variations in fluid and electrolyte status during and in dialysis-free periods may predispose patients to Sudden Cardiac Death (SCD). We studied SCD in HD in relation to the interdialytic interval in patients on a twice-weekly HD schedule.</p><p><strong>Method: </strong>An ambispective cohort study was done and data of HD patients on twice-weekly schedule were collected from January 2009 to December 2017. Primary outcome was cardiovascular mortality and secondary outcome was estimate of standard mortality ratio (SMR) at each 12-hour (h) period interval of the HD schedule. Deaths were categorized as Sudden Cardiac Death, non-Sudden Cardiac Death, and non-Cardiac Death as per standard definitions.</p><p><strong>Results: </strong>Of 413 participants, 289 died. The rates of Cardiovascular death accounted for 121 (42%), and non-cardiac death was 168 (58.1%) respectively SCD was the most common cardiovascular event, accounting for 83 (28.7%) of overall mortality. SCD is more likely to occur in the first 12 hours after dialysis following the 3 days long interdialytic interval (SMR: 2.04) and in the 12 hours before the next dialysis session after a short interval (SMR: 1.74).</p><p><strong>Conclusion: </strong>Occurrence of SCD was higher at two different time points, i.e. 12h period from starting with the dialysis procedure and 12 h period before the start of the next session of HD at the end of a short interval.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-18"},"PeriodicalIF":2.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Link between Hypertension and Cerebral White Matter Changes in Chronic Kidney Disease.","authors":"Kung-Chao Chen, Feng-Ching Shen, Wen-Ching Chen, Hsiu-Fen Lin, Teng-Hui Huang, Ming-Yen Lin, Shu-Li Wang, Fan-Pei Gloria Yang, Mei-Chuan Kuo, Yi-Wen Chiu, Shang-Jyh Hwang, Ping-Hsun Wu, Yi-Ting Lin","doi":"10.1159/000545890","DOIUrl":"https://doi.org/10.1159/000545890","url":null,"abstract":"<p><strong>Background: </strong>Patients diagnosed with chronic kidney disease (CKD) are at a higher risk of encephalopathy, a condition exacerbated by the presence of various chronic diseases. Hypertension is a significant risk factor for brain damage in the general population but is limitedly discussed in patients with CKD. Brain Magnetic Resonance Imaging (MRI) is an excellent tool for evaluating cerebral white matter lesions. Most previous studies showed the association between hypertension and cerebral white matter lesions in the general population but were less focused on CKD patients. Therefore, the present study aims to investigate the effect of hypertension on the cerebral white matter lesions of brain MRI in patients with CKD.</p><p><strong>Methods: </strong>In this retrospective study, we enrolled 1,749 CKD patients who underwent brain MRIs to evaluate their brain lesions in Kaohsiung Medical University Hospital. The cerebral white matter hyperintensities (WMHs) on MRI were evaluated according to the Fazekas scale, including separate periventricular and deep white matter lesions from grade 0 to grade 3. The multivariable ordinal regression model was analyzed to determine the independent association between hypertension or blood pressure and cerebral WMHs with adjustment of controlling age, sex, education, comorbidities (hyperlipidemia, cerebrovascular disease, chronic heart failure), laboratory data (hemoglobin, albumin, triglyceride, estimated glomerular filtration rate).</p><p><strong>Results: </strong>Hypertension was associated with the Fazekas scale of periventricular lesions in multivariable-adjusted ordinal regression analysis (odds ratio [OR] 1.63, 95% confidence interval [CI] 1.15-2.30) after full adjustment. However, the hypertension comorbidities did not associate with the Fazekas scale of deep white matter lesions in the fully adjusted model (OR 1.24, 95% CI [0.89-1.75]). A positive association between blood pressure (per 10 mmHg increase) and the Fazekas scale was mainly on diastolic blood pressure (DBP) rather than systolic blood pressure (SBP).</p><p><strong>Conclusions: </strong>In CKD patients, hypertension was associated with brain white matter damage, in particular, Fazekas scale of periventricular lesions. Further study is needed to evaluate adequate blood pressure control to decrease the risk of brain damage in CKD patients.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-29"},"PeriodicalIF":2.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thromboxane A2 or activated platelets slightly low-er Fgf23 expression in vitro.","authors":"Elena Kohm, Steffen Rausch, Julia Vogt, Martina Feger, Michael Föller","doi":"10.1159/000545696","DOIUrl":"https://doi.org/10.1159/000545696","url":null,"abstract":"<p><strong>Introduction: </strong>Fibroblast growth factor 23 (FGF23) has emerged as an important endocrine regulator of renal phosphate and vitamin D metabolism and as a factor implicated in patho-physiological processes in further organs including heart. In myocardial infarction, elevations of plasma FGF23 can be observed that may be related to left ventricular hypertrophy or fibro-sis. A critical event in the development of myocardial infarction and thrombosis is platelet aggregation due to thromboxane A2 (TxA2) formation. We studied whether TxA2 is a regula-tor of FGF23.</p><p><strong>Methods: </strong>Experiments were performed in rat UMR-106 osteoblast-like cells and mouse MC3T3-E1 upon exposure to TxA2, pharmacological manipulation of TxA2 sig-naling, or co-incubation with platelets isolated from healthy volunteers. Fgf23 transcripts were analyzed by qRT-PCR and FGF23 protein by ELISA.</p><p><strong>Results: </strong>As a result, TxA2 or stable TxA2 receptor agonists I-BOP or U46619 significantly suppressed Fgf23 gene expres-sion, an effect abrogated by TxA2 receptor antagonist SQ29548. TxA2 signaling also down-regulated FGF23 protein concentration in the cell culture supernatant. Co-incubation of UMR-106 cells with freshly isolated human thrombocytes activated with thrombin, but not with non-activated platelets or thrombin alone significantly lowered Fgf23 gene expression in UMR-106 cells.</p><p><strong>Conclusion: </strong>Taken together, TxA2 signaling suppresses FGF23 production in UMR-106 and MC3T3-E1 bone cells. TxA2-dependent regulation of FGF23 synthesis may be particularly relevant for common diseases associated with enhanced platelet aggregation.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-23"},"PeriodicalIF":2.3,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New drugs available for Fabry disease.","authors":"Fernando Perretta, Gustavo Cabrera, Juan Politei","doi":"10.1159/000546152","DOIUrl":"https://doi.org/10.1159/000546152","url":null,"abstract":"<p><strong>Background: </strong>Fabry disease (FD) is an X-linked genetic condition caused by variants in the GLA gene, leading to a deficiency of the lysosomal enzyme α-galactosidase A (α-Gal A) and the accumulation of complex glycosphingolipids such as globotriaosylceramide (Gb3) and globotriaosylsphingosine (Lyso-Gb3). The systemic disorder primarily affects the cardiovascular, renal, and nervous systems, resulting in decreased life expectancy. The timing of treatment initiation and optimal dosing play crucial roles in improving outcomes and quality of life (QoL) in Fabry patients. Available FD treatments include enzyme replacement therapy (ERT) with agalsidase alfa, aglasidase beta, and pegunigalsidase alfa, as well as oral chaperone therapy with migalastat, which can all stabilize or reduce the disease burden.</p><p><strong>Summary: </strong>This review focuses exclusively on newly available drugs and future therapeutic approaches for treating FD, including migalastat, pegunigalsidase alfa, substrate reduction therapy (SRT), and gene therapy. Migalastat provides benefits such as oral administration and non-immunogenicity; however, it is only appropriate for patients with \"amenable\" GLA variants. The recently approved pegunigalsidase alfa is a pegylated form of α-Gal A manufactured in plant cell cultures, with apparent reduced immune response and prolonged circulating half-life. SRT (venglustat, lucerastat) reduces Gb3 synthesis, helping to normalize metabolic processes while offering certain advantages such as oral administration, non-immunogenic properties, and the possible crossing of the blood-brain barrier. Clinical trials in human and animal model studies are currently investigating ex-vivo and in-vivo gene therapy techniques, showing positive early outcomes. Messages: The ongoing development of novel treatments for Fabry disease suggests that patients will soon have access to a wider array of therapies, enabling more individualized care approaches. Although a definitive FD cure hasn't been achieved and the expense of combining therapies remains challenging, new therapeutic options such as gene and mRNA-based treatments show promise, though more research is needed.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-17"},"PeriodicalIF":2.3,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphological analysis of podocyte injury and death in primary IgA nephropathy.","authors":"Maria Luíza Gonçalves Dos Reis Monteiro, Laura Penna Rocha, Luísa Almeida Sarti Vasconcellos, Lucas Fernandes Pinheiro, Rosiane Nascimento Alves, Aline Cristina Souza da Silva, Liliane Silvano Araújo, Crislaine Aparecida Silva, Marlene Antônia Reis, Juliana Reis Machado","doi":"10.1159/000545841","DOIUrl":"https://doi.org/10.1159/000545841","url":null,"abstract":"<p><strong>Introduction: </strong>IgA nephropathy (IgAN) is characterized by hematuria but can present with different clinical presentations. Proteinuria has been reported as the most important risk factor for the progression of IgAN and it may be related to podocyte injury.</p><p><strong>Methods: </strong>The kidney biopsy samples from patients with IgAN were analyzed using immunohistochemistry for WT1 to determine podocyte density and Transmission Electron Microscopy to assess ultrastructural changes in podocytes and adjacent structures. A comparative group of patients diagnosed with minimal change disease (MCD) and a control group of autopsy samples without kidney disease were included.</p><p><strong>Results: </strong>Slit diaphragm density was lower in IgAN cases compared to controls but higher than in MCD cases. Podocyte density was significantly lower in the IgAN and MCD groups compared to controls, with the MCD group showing even lower density than the IgAN group. Podocyte density was lower in cases with nephrotic proteinuria both in MCD and IgAN. A significant negative correlation was detected between podocyte density and proteinuria in both conditions. A significantly lower proportion of detached podocytes was observed in cases with isolated autophagy and cases with autophagy showed a lower frequency of hematuria and a higher percentage of T0.</p><p><strong>Conclusion: </strong>We demonstrated that podocyte alterations in IgA nephropathy (IgAN) correlate with clinical parameters, including nephrotic proteinuria, hematuria, and interstitial fibrosis. Podocyte loss was associated with necrosis and mitotic catastrophe, while autophagy was prevalent but not apoptosis. Autophagy appears to protect against podocyte detachment. These findings highlight pathophysiological mechanisms relevant to diagnostic and clinical practice.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"1-24"},"PeriodicalIF":2.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}