Badr Khbouz, Nicola Wanner, Laurel Damashek, Tobias B Huber
{"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":"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. 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 toward 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}
Maria J Vargas-Brochero, Anila Cara, Andrea Angioi, Nicola Lepori, Roberta Fenoglio, Francesca Bertinetto, Cristián Juanet, Pilar Acuña Aguayo, Helio Vida Cassi, Trisha Laxamana, Ladan Zand, Loren Herrera Hernandez, Sanjeev Sethi, Cynthia S Crowson, Savino Sciascia, Eduardo Gutiérrez, Ángel Sevillano, Luciana Andrade, Rosanna Coppo, Richard Glassock, Antonello Pani, Dario Roccatello, Fernando Caravaca-Fontán, Fernando C Fervenza
{"title":"A multi-center cohort study evaluated hemoglobinuria as a marker of inflammation in IgA nephropathy.","authors":"Maria J Vargas-Brochero, Anila Cara, Andrea Angioi, Nicola Lepori, Roberta Fenoglio, Francesca Bertinetto, Cristián Juanet, Pilar Acuña Aguayo, Helio Vida Cassi, Trisha Laxamana, Ladan Zand, Loren Herrera Hernandez, Sanjeev Sethi, Cynthia S Crowson, Savino Sciascia, Eduardo Gutiérrez, Ángel Sevillano, Luciana Andrade, Rosanna Coppo, Richard Glassock, Antonello Pani, Dario Roccatello, Fernando Caravaca-Fontán, Fernando C Fervenza","doi":"10.1016/j.kint.2026.07.021","DOIUrl":"10.1016/j.kint.2026.07.021","url":null,"abstract":"<p><strong>Introduction: </strong>Hematuria is a hallmark clinical manifestation of IgA nephropathy (IgAN) and largely reflects underlying glomerular inflammation. Despite this, current guidelines prioritize proteinuria and estimated glomerular filtration rate for risk assessment, and the association between urinary findings and underlying histologic lesions remains incompletely characterized.</p><p><strong>Methods: </strong>Here, we conducted a multicenter retrospective cohort study of patients with biopsy-proven IgAN (July 2015-July 2025) with concurrent urinalysis. Associations between hemoglobinuria (dipstick), hematuria (microscopy), proteinuria and individual Oxford Classification MEST-C components, and composite inflammatory lesions (M1, E1, and/or C1/C2; and E1 and/or C1/C2) were evaluated using unadjusted cohort-specific logistic regression models. Pooled odds ratios (ORs) were estimated using random-effects meta-analysis.</p><p><strong>Results: </strong>Among 441 patients, hemoglobinuria was associated with M1 lesions (pooled OR 1.77, 95% CI 1.25-2.51), E1 lesions (1.75, 1.44-2.11), and crescentic lesions (1.57, 1.20-2.07). Hematuria was also associated with M1 lesions (1.24, 1.14-1.35), E1 lesions (1.22, 1.13-1.31), and C1/C2 lesions (1.18, 1.09-1.28). For the composite outcome (M1, E1, and/or C1/C2), pooled ORs were 2.28 (1.76-2.97) for hemoglobinuria, 1.36 (1.22-1.51) for hematuria, and 1.20 (1.04-1.38) for proteinuria. Hemoglobinuria and hematuria were not associated with chronic lesions, whereas proteinuria was consistently associated with T1/T2 lesions (1.35, 1.20-1.52).</p><p><strong>Conclusions: </strong>Dipstick hemoglobinuria is associated with histologic markers of active disease in IgAN and may provide clinically relevant information to complement current assessment of disease activity in IgAN.</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":"148795051","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}
Silvia M Titan, Andrew D Rule, Janet E Olson, Joshua T Bublitz, Tony C Luehrs, Robert A Vierkant, Hugues Sicotte, Konstantinos N Lazaridis, Vesna D Garovic, Alexandre C Pereira
{"title":"Genetic determinants of serum creatinine and cystatin C independent of kidney function generate bias in filtration markers.","authors":"Silvia M Titan, Andrew D Rule, Janet E Olson, Joshua T Bublitz, Tony C Luehrs, Robert A Vierkant, Hugues Sicotte, Konstantinos N Lazaridis, Vesna D Garovic, Alexandre C Pereira","doi":"10.1016/j.kint.2026.07.018","DOIUrl":"10.1016/j.kint.2026.07.018","url":null,"abstract":"<p><strong>Introduction: </strong>Non-GFR determinants of filtration markers reduce the accuracy of estimated GFR (eGFR) and genetic factors may explain part of this reduced performance. Here, we identify genetic variants associated with serum levels of creatinine or cystatin C (but not GFR), compute their effect, and investigate candidate genes.</p><p><strong>Methods: </strong>We used data from the UK Biobank (approximately 470,000 people) and the CKD-EPI creatinine (eGFRcr) and cystatin C (eGFRcys) equations. Using genome-wide association studies (GWAS), we defined strict criteria to classify loci as creatinine-specific or cystatin C-specific, refined with co-localization studies, and identified associated pathways. We computed biomarker and eGFR polygenic scores as the cumulative effect of biomarker-specific loci (genetic bias) and tested their associations to surrogate markers of identified pathways. Findings were validated by independent studies with measured GFR and mapped candidate genes using expression quantitative trait loci (eQTL) resources.</p><p><strong>Results: </strong>We identified 52 creatinine-specific and 48 cystatin C-specific loci. Using eQTLs to identify candidate causal genes, enriched pathways were energy and muscle metabolism for creatinine, and inflammatory response, cancer, cysteine endopeptidase activity, wound healing, and immune modulatory functions for cystatin C. Polygenic scores showed that individual-level genetic bias in eGFRcr and eGFRcys had mean values of 3.8 (standard deviation 0.94, range -1.5 to 7.9) mL/min per 1.73m<sup>2</sup> and 0.6 (standard deviation 0.93, range -3.5 to 4.7) mL/min per 1.73m<sup>2</sup> , respectively. Genetic bias was different per self-reported race for creatinine and correlated with surrogate markers of selected pathways (muscle mass, for creatinine; body mass index and C-reactive protein, for cystatin C). Lastly, we showed that the difference between polygenic scores derived from GWAS with and without adjustments for the biomarker-specific variants was associated with GFR bias in two independent cohorts (1304 and 939 individuals).</p><p><strong>Conclusions: </strong>Our study identified loci related to serum creatinine or cystatin C but not to GFR and quantified the populational and individual-level effect of genetic determinants on filtration markers and eGFRs.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795114","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":"Chronic kidney disease risk stratification using a proteomic risk score in apolipoprotein L1-mediated kidney disease.","authors":"Pukhraj S Gaheer, Matthew B Lanktree","doi":"10.1016/j.kint.2026.06.048","DOIUrl":"10.1016/j.kint.2026.06.048","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759873","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":"Triple immunosuppressive therapy in active lupus nephritis: does one therapy really fit all?","authors":"Jürgen Floege","doi":"10.1016/j.kint.2026.07.003","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.003","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673729","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":"Better guidelines, better patient lives: a sustainable partnership model for integrating lived experience into clinical guideline development.","authors":"Bill Wang, Nicole Scholes-Robertson","doi":"10.1016/j.kint.2026.02.046","DOIUrl":"10.1016/j.kint.2026.02.046","url":null,"abstract":"<p><p>To realize their full potential in improving health outcomes, clinical guidelines must integrate methodological rigor with practical relevance and human impact. This paper is a work of advocacy and a proposal for action. Drawing on established research, emerging paradigms, and our collective experience as patients and researchers as well as our respective backgrounds in legal, governance, and healthcare, we build a case that the systematic integration of lived experience-the unique embodied knowledge held by patients and caregivers-is essential for guideline relevance and implementation. Distinct from, yet complementary to, clinical and methodological knowledge, this expertise answers \"What is it like?\" and \"What matters?\" Its integration refines topic selection, enriches evidence interpretation, shapes implementable recommendations, and sustains guidelines as living documents for shared decision-making. To move beyond ad hoc involvement, we propose a structured dual framework: a formal Patient and Public Engagement Policy and a sustainable Patient Partner Talent Pipeline for lived experience. The proposed 4-stage pipeline (discovery, apprenticeship, mastery, and stewardship) cultivates lived experience as a professional competency, embedding it from scoping through implementation and governance. A phased implementation plan (codesign, pilot, and scale-up) is outlined to translate this framework into practice. Although framed within the context of Kidney Disease: Improving Global Outcomes (KDIGO), the model is designed for adaptation by any guideline body. The proposed framework offers a structured, actionable, and adaptable method for operationalizing this knowledge, promoting equity, partnership, and guideline impact globally. We present it as a starting point for action and iterative learning, designed to be implemented, evaluated, and refined by the global kidney community and ultimately to better patient lives.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603978","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}