Kidney international最新文献

{"title":"Radiopaque intestinal cast of sodium zirconium cyclosilicate on CT.","authors":"Jia Hui Lan, Hua Ming Wang, Bao-Ping Xu","doi":"10.1016/j.kint.2026.07.020","DOIUrl":"10.1016/j.kint.2026.07.020","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":"148795130","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 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}

{"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 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 1.73m² and 0.6 (standard deviation 0.93, range -3.5 to 4.7) mL/min per 1.73m² , 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":"Combining dietary fiber inulin with parathyroid hormone-lowering therapy improves bone remodeling and mechanics in a rat model of Chronic Kidney Disease–Mineral Bone Disorder","authors":"Matthew R. Allen, Corinne E. Metzger, Neal X. Chen, Shruthi Srinivasan, Kalisha O'Neill, Hannah E. Wilson, Karis Blacklock, Emily K. Matter, Daniel J. Stephen, Karisa M. Ecker, Ariana Moffitt, Annabel Biruete, Sharon M. Moe","doi":"10.1016/j.kint.2026.07.017","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.017","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"2 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148754700","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":"Generation of a novel Slc7a9G105R mutant mouse identifies new biomarkers for cystinuria","authors":"Nirmal P. Bhatt, Theresa T.H. Nguyen, Giulia Iacono, Gabriel R. Rodriguez, Connor R.B. Anderson, Andrew Perry, Christopher K. Barlow, Dovile Anderson, Gaetan Burgio, Benjamin J. Marsland, Simon H. Jiang, Aniruddh V. Deshpande, Malcolm R. Starkey","doi":"10.1016/j.kint.2026.06.050","DOIUrl":"https://doi.org/10.1016/j.kint.2026.06.050","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"9 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148754699","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":"Heme-induced kallikrein-kinin system activation in hemolytic uremic syndrome.","authors":"Alexandra Gerogianni, Niklas Friberg, Markus Wendler, Sára Kellnerová, Alex Antill, Ann-Charlotte Kristoffersson, Johan Flygare, Ida Arvidsson, Diana Karpman","doi":"10.1016/j.kint.2026.05.034","DOIUrl":"10.1016/j.kint.2026.05.034","url":null,"abstract":"<p><strong>Introduction: </strong>Heme is released from red blood cells during hemolytic uremic syndrome (HUS). Here, we investigated hemolysis-induced kallikrein-kinin system activation and the interaction between heme and clotting factor XII (FXII).</p><p><strong>Methods: </strong>Pediatric patients (19 male and 15 female, median age three years, range three months to 14 years) with HUS induced by enterohemorrhagic Escherichia coli (EHEC) and mice infected with EHEC were assessed for activation of the kallikrein-kinin system by degradation of high-molecular-weight kininogen ((HK) by immunoblotting) and levels of residual pre-kallikrein (by chromogenic assay). Heme induction of kallikrein-kinin system activation was evaluated by plasma kallikrein or FXII activity, bradykinin release (by ELISA) and heme binding to FXII (by surface plasmon resonance). Hemolysis was induced in vitro and in mice by phenylhydrazine in the presence or absence of C1-inhibitor.</p><p><strong>Results: </strong>Ten of the 34 patients with EHEC-HUS had HK degradation associated with the severity of hemolysis and 17 of 32 had reduced residual pre-kallikrein associated with kidney dysfunction. Similarly, EHEC-infected mice had HK degradation and pre-kallikrein consumption, the latter inversely correlated with hemolysis biomarkers lactic dehydrogenase and arginase 1 and with creatinine levels. Heme bound to and activated FXII with increased kallikrein activity, causing HK breakdown and releasing bradykinin in normal, but not FXII-deficient plasma; effects inhibited by hemopexin, C1-inhibitor, and corn trypsin inhibitor. Phenylhydrazine-induced hemolysis led to HK degradation in human and murine blood; not detected when red blood cells were added to FXII-deficient plasma, or in the presence of C1-inhibitor. Mice challenged with phenylhydrazine exhibited hemolysis and significant pre-kallikrein consumption as well as HK degradation in five of 10 mice. HK degradation was abrogated by pretreatment with C1-inhibitor.</p><p><strong>Conclusions: </strong>Our study demonstrates that heme binds to and activates FXII leading to HK degradation and bradykinin release. This could be a potent inflammatory mechanism in hemolytic disease, such as HUS, and amenable to pharmacological blockade.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679093","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":"Podocin oligomerization links slit-diaphragm architecture and NPHS2 genetics","authors":"Florian Grahammer, Achilleas S. Frangakis","doi":"10.1016/j.kint.2026.07.008","DOIUrl":"https://doi.org/10.1016/j.kint.2026.07.008","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"113 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148767553","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":"Front-loading response: why combination therapy should anchor initial lupus nephritis treatment.","authors":"Juan M Mejia-Vilet, Isabelle Ayoub","doi":"10.1016/j.kint.2026.04.043","DOIUrl":"https://doi.org/10.1016/j.kint.2026.04.043","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":"148673685","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}