Kidney international最新文献

{"title":"Skeletal oxalosis in a child on maintenance hemodialysis.","authors":"Zhengwen Xing, Ping Wang, Xiaoe Zhang, Liyin Zhang, Yulin Kang, Weihua Zheng, Shaojun Liu, Ying Wu","doi":"10.1016/j.kint.2026.08.009","DOIUrl":"https://doi.org/10.1016/j.kint.2026.08.009","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Invisible Bladder Stone Causing Silent Obstructive Kidney Failure.","authors":"Jing-Huan Liao, Chin-Li Chen, Shun-Neng Hsu","doi":"10.1016/j.kint.2026.08.011","DOIUrl":"https://doi.org/10.1016/j.kint.2026.08.011","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Polycystic Kidney as a Staphylococcal Reservoir.","authors":"Juliette Leon, Pauline Brocard, Clara Tescher, Guillaume Reichert, Antoine Troger, Dany Anglicheau, Aurélie Hummel, Dominique Joly","doi":"10.1016/j.kint.2026.08.010","DOIUrl":"https://doi.org/10.1016/j.kint.2026.08.010","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asia-Pacific Summit on Implementation of Clinical Practice Guidelines on Diabetes and Blood Pressure Management in Chronic Kidney Disease: A KDIGO Summit Report.","authors":"Angela Yee-Moon Wang, Sinee Disthabanchong, Kei Fukami, Tazeen H Jafar, Hyeong Cheon Park, Sunita Bavanandan","doi":"10.1016/j.kint.2026.07.027","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.027","url":null,"abstract":"<p><strong>Kidney disease: </strong>Improving Global Outcomes (KDIGO) has published the Clinical Practice Guidelines (CPG) on managing diabetes in CKD in 2022 and the CPG for managing blood pressure in CKD in 2020. KDIGO organized a guideline implementation summit targeting the Asia-Pacific region in Kuala Lumpur in 2024 with the aim to understand existing barriers and challenges in implementation of the two CPGs and to propose possible solutions, tailored to the country or region's income level to bridge existing gaps in guideline implementation. The implementation summit discussion covered 4 key themes: i) lifestyle intervention; ii) adoption of comprehensive team-based integrated care model; iii) achievement of various treatment targets albuminuria screening and monitoring of kidney disease; and iv) implementation of guideline-directed medical therapies. The Summit was attended by co-chairs of the KDIGO CPGs on diabetes and blood pressure management in CKD, with nephrologists, endocrinologists, primary care physicians, dietitians, a health economist, and patient partners from 13 Asia-Pacific countries or regions. This conference report summarizes the key challenges in the CPG implementation for diabetes, hypertension in people with CKD in Asia-Pacific region, and provides a strategic framework of actions to overcome these barriers.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SEISMIC: A multi-stakeholder summit addressing access issues in diagnosis and treatment of C3G nephropathy and IC-MPGN.","authors":"Carla Nester, Joshua Tarnoff, Susan Brisendine, Laurel Damashek, Angel Morales, Lindsey Fuller, Marianne Silkjaer Nielsen, Giulia Bassanese, David Feldman, Daniel P Gale, Tobias B Huber, David Kavanagh, Antonia King, Doug Paul, Matthew Pickering, Brad Rovin, Aditi Sinha, Richard J H Smith, Fabrizio Spoleti, Patrick D Walker, Jack F Wetzels, Howard Trachtman, Marina Vivarelli","doi":"10.1016/j.kint.2026.07.024","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.024","url":null,"abstract":"<p><p>C3 glomerulopathy-primary immune complex membranoproliferative glomerulonephritis (C3G/IC-MPGN) is an ultrarare disease spectrum associated with a significant health burden and for which there is a huge unmet need for safe and effective treatment. The underlying pathophysiology is dysregulation and overactivation of the alternative complement pathway. Two new therapeutic agents, iptacoplan and pegcetacoplan, that target proximal steps in the cascade, have demonstrated to be effective and have been approved for use in patients with C3G alone and with C3G/IC-MPGN, respectively. A key challenge to the nephrology community is how to incorporate these disease-modifying drugs into clinical practice in a timely and equitable manner. This report summarizes the deliberations and recommendations that emerged from the SEISMIC (Addressing access issues in diagnosis and treatment of C3G nephropathy and IC-MPGN) summit in July 2025. The meeting assembled a broad panel of experts and patients and addressed the following three aims: 1) define issues in proper and timely diagnosis of this complex disease spectrum, 2) assess management strategies in light of the availability of this new class of therapeutic agents, and 3) identify barriers to access to care and treatment with these new therapeutic agents and design strategies to surmount them.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outcomes from the International Society of Nephrology Forum on Complement Therapeutics in C3G & IgAN.","authors":"D Kavanagh, A Alladin-Karan, S Alexander, S Chauvet, C K Cheung, H T Cook, F Fakhouri, V Fremeaux-Bacchi, D P Gale, P Garred, R A Lafayette, A L T Ma, C Nester, R J H Smith, E Pillebout, H N Reich, D V Rizk, I S D Roberts, B H Rovin, S H Sacks, S Shah, H Trimarchi, M Vivarelli, E K S Wong, H Zhang, J Barratt","doi":"10.1016/j.kint.2026.08.007","DOIUrl":"https://doi.org/10.1016/j.kint.2026.08.007","url":null,"abstract":"<p><p>C3 glomerulopathy (C3G) and primary immune-complex membranoproliferative glomerulonephritis (IC-MPGN) are both prototypical complement disorders in which complement overactivation is the primary driver of disease. Complement is not the primary cause of disease in IgA nephropathy (IgAN); however, increasing evidence implicates complement as a secondary factor in kidney damage in this more complex, multifactorial disorder. The success of recent clinical trials using alternative pathway complement inhibitors in C3G, IC-MPGN, and IgAN pose questions as to how they should be used in the real world. We report the findings of the 2025 International Society of Nephrology Forum on Complement Therapeutics in C3G & IgAN, where a global panel of experts considered the current state of knowledge, identified areas of uncertainty, and proposed optimal solutions. Areas of uncertainty and areas for future research included how complement biomarkers, complement autoantibodies, genetics and the kidney biopsy guide therapy. The current rationale for the use of complement inhibitors and their place within the current therapeutic landscape are discussed.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving the Histologic Classification of Advanced Diabetic Nephropathy Based on the Transformative Research in Diabetic Nephropathy (TRIDENT) Findings.","authors":"Samer Mohandes, Cynthia C Nast, Amy Mottl, Julia Scialla, Salem Almaani, Randy Luciano, Tamara Isakova, Carla Ellis, Shweta Bansal, Christos Argyropoulos, J Charles Jennette, Adil Gasim, Isaac E Stillman, Kirk N Campbell, Amin Abedini, Gaia Coppock, Katalin Susztak, Matthew B Palmer","doi":"10.1016/j.kint.2026.07.028","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.028","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic nephropathy (DN) remains the leading cause of kidney failure worldwide. Histopathologic assessment is the diagnostic standard, and the Renal Pathology Society (RPS) classification system is widely used in clinical practice and research. However, its prognostic performance is limited, particularly in advanced disease.</p><p><strong>Methods: </strong>To examine this, we used TRIDENT, a multicenter, prospective observational cohort of patients with diabetes undergoing clinically indicated kidney biopsy (176 individuals). Light-microscopy features were scored and analyzed by unsupervised k-means clustering to derive the RPS-TRIDENT modification (RPS-TM) classification. Associations between RPS-TM classes and kidney outcomes: death, dialysis initiation or 40% or more decline in estimated glomerular filtration rate were evaluated with Kaplan-Meier curves and Cox proportional hazards models. Clinical utility was assessed by decision-curve analysis. An external cohort of 101 individuals was used for validation.</p><p><strong>Results: </strong>The RPS classification showed only modest prognostic discrimination, with no significant survival difference between classes 3 and 4. The RPS-TM classification introduced an additional high-risk category (Class 5) defined by visceral epithelial hyperplasia, which more clearly separated risk groups, modestly improved prediction at one year (area under the curve 0.68 vs. 0.65) and two years (0.75 vs. 0.71), and demonstrated higher net benefit in decision curve analysis. RPS-TM Class 5 had the most rapid progression to kidney failure.</p><p><strong>Conclusions: </strong>The RPS-TM classification enhances prognostication in DN by identifying a morphologic subgroup characterized by visceral epithelial hyperplasia with aggressive clinical course. This framework offers more precise risk stratification and could guide targeted management and trial design in DN.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From podocyte biology to glomerular medicine: The 15th International Podocyte Conference 2025.","authors":"Badr Khbouz, Nicola Wanner, Laurel Damashek, Tobias B Huber","doi":"10.1016/j.kint.2026.07.026","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.026","url":null,"abstract":"<p><p>The 15th International Podocyte Conference was held in Hamburg, Germany from June 10 to 13, 2025, marking the inaugural meeting of the International Society of Glomerular Disease (ISGD). The conference opened with a vibrant Pre-Meeting Day for Emerging Career Researchers, featuring early-career talks and exchanges on scientific and career development. The main program reflected the evolution of the field and underscored the rationale for a sustained focus on podocyte biology. Key insights included the need to shift from a disease-oriented model towards glomerular health, the complexity of glomerular cell types and interactions, and advances in identifying causal genes in kidney function through genetic studies. Unmet needs were also emphasized around patient experience, access to expert care, and trial design. Serving as a report from the 15th International Podocyte Conference, this review captures the evolving landscape of podocyte and glomerular disease research as discussed by the global scientific community.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eruptive disseminated porokeratosis after kidney transplantation.","authors":"Pablo Balado-Simó, Daniel Morgado-Carrasco","doi":"10.1016/j.kint.2026.08.003","DOIUrl":"10.1016/j.kint.2026.08.003","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A self-sustaining hypoxia inducible factor-1α-creatine kinase B feedforward circuit drives macrophage-mediated kidney fibrosis.","authors":"Tingting Xie, Hao Qi, Piaoyu Dai, Changhan Chen, Yiyan Wang, Zhenjiang Li, Weilun Huang, Wuping Liu, Mengzhi Wu, Yujin Zhang, Ziqing Gao, Haosen Xu, Lijun Zuo, Qingyang Liu, Benjamin C Brown, Angelo D'Alessandro, Rodney E Kellems, Weiru Zhang, Yang Xia","doi":"10.1016/j.kint.2026.07.019","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.019","url":null,"abstract":"<p><strong>Introduction: </strong>A fundamental challenge in treating chronic kidney disease (CKD) is the lack of therapies to reverse established fibrosis. While systemic hypoxia sensors like erythrocyte sphingosine kinase 1 (eSPHK1) can initiate fibrotic signaling, the mechanisms driving self-perpetuating and progressive fibrosis remain unknown.</p><p><strong>Methods: </strong>eSphk1 specific deficient mice underwent four-week angiotensin-II infusion, unilateral ureteral obstruction or ischemia reperfusion injury. Untargeted metabolomics profiled purified kidney macrophages, and [¹³C₆¹⁵N₄]-arginine fluxomic tracked arginine-creatine metabolism in hypoxia treated macrophages. Multi-color immunofluorescent images of kidney tissues were scanned and scored. Preclinical studies by hypoxia inducible factor-1α (HIF-1α) inhibitor or knockdown macrophage creatine kinase B (Ckb) were performed. Clinical relevance was evaluated by measuring CKB mRNA level in peripheral blood mononuclear cells obtained from 131 patients with CKD and determining its correlation with disease severity.</p><p><strong>Results: </strong>We identify a HIF-1α-CKB feedforward loop within profibrotic macrophages that functions as an autonomous engine of kidney fibrosis. This circuit, which can be triggered by established pathways such as eSphk1 dysfunction, is characterized by its capacity for self-renewal. Specifically, HIF-1α drives Ckb expression, reprogramming arginine metabolism toward creatine phosphate shunt (CPS) to generate an ATP surge that synergizes with an S1PR3-PKC signaling cascade to phosphorylate and stabilize HIF-1α, effectively bypassing the need for continued hypoxic input. This metabolic rewiring drives macrophage profibrotic polarization and leads to kidney fibrosis. Preclinically, pharmacologic HIF 1α inhibition or knockdown macrophage Ckb collapses this autonomous loop and halts fibrosis. Translationally, CKB mRNA in peripheral blood mononuclear cells rises in parallel with estimated glomerular filtration rate decline and histologic fibrosis score in patients with CKD.</p><p><strong>Conclusions: </strong>Our work identifies a novel HIF-1α-CKB feedforward circuit in macrophages that sustains HIF-1α induction, channeling arginine metabolism toward CPS and thus promoting kidney fibrosis. These findings highlight that fibrosis is conceptualized from a passive end-stage outcome to an actively maintained process driven by the macrophage metabolic-polarization circuit, suggesting that breaking this malicious loop, in addition to initiating triggers, is critical to halt kidney fibrosis.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}