Journal of The American Society of Nephrology最新文献

{"title":"Spatially Distinct TREM2+ Macrophages Are Associated with Compartment-Specific Protection in Diabetic Kidney Disease.","authors":"Jia Fu, Yangyang Niu, Dongyuan Chang, Zeguo Sun, Benjamin Lo, Wenlin Wang, Pinhong Wu, Jessica Liu, Wei Cai, Weijia Zhang, Kyung Lee, John Cijiang He","doi":"10.1681/ASN.0000001248","DOIUrl":"https://doi.org/10.1681/ASN.0000001248","url":null,"abstract":"<p><strong>Background: </strong>Diabetic kidney disease (DKD) is driven by complex pathological mechanisms including lipid accumulation, chronic inflammation, and fibrosis, contributing to progressive kidney dysfunction. Macrophages are key contributors to DKD pathogenesis, yet their functional heterogeneity in the diabetic kidney remains poorly defined. While TREM2+ macrophages have been identified within the diabetic microenvironment, the relationship between their developmental origin, anatomical localization, and functional specialization remains unclear.</p><p><strong>Methods: </strong>In this study, we integrated single cell-RNA sequencing, spatial transcriptomic analysis of diabetic OVE26 kidneys, and reciprocal bone marrow transplantation in a high fat diet plus streptozotocin-induced diabetic model to examine how TREM2+ macrophages are distributed across renal compartments and how TREM2 deficiency affects DKD injury.</p><p><strong>Results: </strong>Global TREM2 deficiency markedly exacerbated tubulointerstitial injury and glomerular hypertrophy in DKD, establishing TREM2 as a protective factor. Single-cell RNA sequencing and spatial mapping revealed that TREM2 induction in diabetic kidneys occurs in two spatially distinct macrophage populations: Mrc1+ kidney-resident macrophages localized to the periglomerular niche, and Ccr2+ monocyte-derived macrophages infiltrating the tubulointerstitium. Transcriptomic and functional analyses were consistent with a role of TREM2 in macrophage phagocytic and lipid-handling programs. Its loss led to the downregulation of phagosome and endocytic pathways, resulting in failed clearance of apoptotic debris and lipid aggregates, which was particularly pronounced in the tubulointerstitium. Reciprocal bone marrow transplant experiments suggest that recipient-resident TREM2 was more associated with preservation of glomerular structure, whereas donor-derived hematopoietic TREM2 was more strongly associated with limiting tubular lipid accumulation, apoptotic tubular epithelial cells, and tubulointerstitial injury.</p><p><strong>Conclusions: </strong>These findings suggested that TREM2-expressing macrophages contributed to compartment-specific protective responses in diabetic kidney disease. TREM2 deficiency was associated with greater diabetic glomerular and tubular injury, with distinct phenotypes observed in donor hematopoietic and recipient compartments.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148969458","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":"Performance of the iBox Prognostication System in African American Kidney Transplant Recipients","authors":"Agathe Truchot,Yannis Lombardi,Marc Raynaud,Olivier Aubert,Gillian Divard,Thibaut Thalamas,Brad Astor,Didier Mandelbrot,Sandesh Parajuli,Kenneth A. Newell,Christian P. Larsen,Geeta Karadkhele,Babak Orandi,John J. Friedewald,Gaurav Gupta,Enver Akalin,Stanley C. Jordan,Arthur J. Matas,Miklos Z. Molnar,Junji Yamauchi,Katalin Fornadi,Andrew J. Bentall,Mark D. Stegall,Roslyn B. Mannon,Dorry L. Segev,Edmund Huang,William E. Fitzsimmons,Alexandre Loupy","doi":"10.1681/asn.0000001247","DOIUrl":"https://doi.org/10.1681/asn.0000001247","url":null,"abstract":"Background: The iBox is a validated prognostication system that predicts long-term death-censored graft loss in kidney transplant recipients, but its performance in the specific population of African American recipients has not been fully studied. Methods: We conducted a multicenter study including 3,866 kidney transplant recipients from North America, of whom 1,040 (27%) were African American, to assess the impact of race on the iBox’s performance in predicting graft loss. Discrimination, calibration, overall fit and clinical utility were evaluated in the whole cohort and in African American and non-African American recipients. Results: Performance metrics for the prediction of graft loss were similar in both subgroups in terms of discrimination (c-index 0.80 [95% CI: 0.77-0.83] in African American recipients and 0.83 [95% CI: 0.81-0.85] in non-African American recipients, p=0.07), and observed/expected ratios (1.08 [95% CI: 0.95-1.23] and 0.99 [95% CI: 0.88-1.10], respectively, p=0.28). No significant interaction between iBox score values and race was found in multivariable analysis stratified by transplant center (p=0.29 for the interaction term). Results were consistent between subgroups regardless of the equation used to estimate glomerular filtration rate (Kidney Recipient Specific [KRS], CKD-EPI, or MDRD), with small variations in calibration across equations. Conclusions: The iBox prognostication system showed accurate discrimination, overall fit, and clinical utility up to 7 years post-risk evaluation in African American and non-African American kidney transplant recipients, supporting its robustness in this population.","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"4 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148923260","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":"Kidney-on-Chip and Organoid Models: Harnessing Mechanical Forces for Translational Kidney Biology.","authors":"Abigail Daily, Nanditha Anandakrishnan, Jonathan Haydak, Jonathan Himmelfarb, Evren U Azeloglu","doi":"10.1681/ASN.0000001272","DOIUrl":"https://doi.org/10.1681/ASN.0000001272","url":null,"abstract":"<p><p>The FDA Modernization Act and the subsequent federal policy changes in 2025 have signaled a shift towards the use of non-animal, human-centered models for preclinical drug development and toxicity screening, emphasizing 3D cell-based, organ-on-chip, and organoid platforms as alternatives to animal models. While animal models have been instrumental in improving our understanding of disease mechanisms, they do not allow decoupling of biomechanical and biochemical effects during pathogenesis. Standard in vitro systems offer improved accessibility but often lack physiologically relevant microenvironments. In this review, we discuss how kidney-on-chip and iPSC-derived kidney organoid models serve as physiologically relevant platforms for modeling nephrotoxicity, kidney development, and pathophysiology. Kidney-on-chip models can recapitulate in vivo mechanical forces, such as fluid shear stress and mechanical strain, experienced by cells, enabling real-time functional readouts of glomerular filtration, tubular reabsorption, and potential nephrotoxic response. Integrating on-chip platforms with patient-derived iPSCs and differentiated kidney cell types allows human-relevant responses unavailable in static culture. iPSC-derived kidney organoids recapitulate the 3D architecture of nephron segments and ureteric bud branching patterns, demonstrating selective transport, toxicity responses, and structural stability over months in culture. We detail how bioengineering approaches, including organoid-on-chip models, bioprinting, and multi-organ-on-chip integration, could address the current limitations of these systems, like maturity, scalability and vascularization. We further discuss how integrating publicly available clinical databases and machine learning approaches with on-chip validation can improve translational relevance. We conclude that interdisciplinary collaboration between engineers, biologists, and physician scientists will be essential to translate bioengineered kidney models into clinical and therapeutic applications.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912626","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":"Quantum Dot-Based Fluorescent Lateral Flow Immunoassay Strip for Rapid Detection of Anti-nephrin Autoantibodies in Idiopathic Nephrotic Syndrome.","authors":"Mingyu Lai, Rui Gu, Jiayi Shen, Tong Shao, Baohua Yang, Jianhua Mao, Qing Ye","doi":"10.1681/ASN.0000001246","DOIUrl":"https://doi.org/10.1681/ASN.0000001246","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic nephrotic syndrome is a common primary glomerular disease in children. Circulating anti-nephrin autoantibodies have emerged as clinically relevant biomarkers, but existing detection methods are complex and time-consuming. We developed a quantum dot microsphere-based lateral flow immunoassay (QD-LFIA) for rapid serum anti-nephrin autoantibody detection.</p><p><strong>Methods: </strong>Quantum dot microspheres were conjugated to recombinant human nephrin protein, and the reading time, T-line coating concentration, and nephrin protein labeling amount were optimized. Analytical performance was evaluated by receiver operating characteristic (ROC) analysis based on test line/control line ratios generated by the dry fluorescence immunoanalyzer, together with interference and accelerated stability testing. Clinical performance was assessed in 191 pediatric serum samples, with qualitative QD-LFIA results compared against immunoprecipitation-Western blotting (IP-WB). Discordant samples were evaluated by recombinant nephrin protein inhibition assay. Clinical indices were compared between anti-nephrin autoantibody positive and negative patients.</p><p><strong>Results: </strong>The optimized reaction time, T-line coating concentration, and recombinant nephrin protein labeling amount were 10 min, 0.5 mg/mL, and 92.4 μg, respectively. ROC analysis yielded an AUC of 0.90 (95% CI 0.84-0.97), with 93% sensitivity and 92% specificity at a test line/control line cutoff of 0.003. The QD-LFIA resisted the tested interferents and maintained stable performance for 40 days at 37 °C. QD-LFIA achieved overall, positive, and negative percent agreements of 92%, 89%, and 93%, respectively, relative to IP-WB. Recombinant nephrin protein inhibition abolished the signals in all 12 QD-LFIA-positive/IP-WB-negative samples. Anti-nephrin autoantibody positive patients had higher 24-h urinary protein excretion and lower serum albumin levels than negative patients.</p><p><strong>Conclusions: </strong>These findings suggest that the QD-LFIA enabled rapid detection of anti-nephrin autoantibodies in children with idiopathic nephrotic syndrome. The QD-LFIA showed good agreement with IP-WB and identified additional anti-nephrin-positive samples undetected by IP-WB.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912691","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":"Macrophage IgG Recycling Couples Glomerular IgG Accumulation to Podocyte Senescence in Obesity-Related Glomerulopathy.","authors":"Zikang Liu, Binbin Dai, Yuxuan Jin, Jiwen Bao, Hanxue Zhao, Yurong Lin, Hongtu Hu, Yangbin Pan","doi":"10.1681/ASN.0000001243","DOIUrl":"https://doi.org/10.1681/ASN.0000001243","url":null,"abstract":"<p><strong>Background: </strong>Obesity-related glomerulopathy is increasingly common, yet its pathogenesis remains poorly understood. This study aimed to elucidate the mechanisms by which nonspecific glomerular IgG deposition promotes podocyte senescence in obesity-related glomerulopathy, thereby expanding potential therapeutic options.</p><p><strong>Methods: </strong>Kidney samples from patients with obesity-related glomerulopathy and diet-induced obese mice were used to compare glomerular IgG localization and abundance in obese versus control states. Causality between glomerular IgG accumulation and podocyte senescence was assessed by exogenous IgG supplementation and B cell deficiency mice. Primary podocytes were IgG-stimulated for transcriptomic and lipidomic profiling, and sphingomyelin phosphodiesterase 3 (Smpd3) was validated by in vitro and in vivo loss-of-function studies. Macrophage-specific FcRn deletion and anti-CD20 therapy were further used to evaluate IgG-targeted strategies for mitigating podocyte senescence and injury in ORG.</p><p><strong>Results: </strong>Glomerular IgG deposition was markedly increased in both patients with obesity-related glomerulopathy and mice with diet-induced obesity. Exogenous IgG supplementation in non-obese mice reproduced the glomerular IgG accumulation and podocyte senescence observed in HFD fed mice. Conversely, B-cell null diet-induced obese mice and anti-CD20 treated diet-induced obese mice showed greatly reduced glomerular IgG levels and attenuated podocyte injury. Mechanistically, IgG exposure activated podocyte sphingolipid metabolism, notably upregulating Smpd3 and increasing intra-podocyte ceramide. In vitro and in vivo Smpd3 knockdown prevented IgG induced ceramide accumulation and podocyte senescence. Obesity also heightened glomerular macrophage infiltration, and macrophage depletion or macrophage-specific FcRn knockout significantly reduced glomerular IgG deposition and protected against podocyte injury and senescence.</p><p><strong>Conclusions: </strong>FcRn-expressing macrophages increased obesity-induced IgG retention in glomeruli, which led to podocyte ceramide overload and senescence.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891893","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":"Risk, Not Just Rate: Toward Individualized Correction in Hyponatremia.","authors":"Harish Seethapathy, Sahir Kalim, Sagar U Nigwekar","doi":"10.1681/ASN.0000001270","DOIUrl":"10.1681/ASN.0000001270","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887928","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":"Chimeric HLA Antibody Receptor (CHAR) T Cells to Specifically Eliminate HLA-DQ-Specific B Cells.","authors":"Carolt Arana, Ilse Gille, Renate Hagedoorn, Ainhoa García-Busquets, Hannah C M Schenk, Sergi Betriu, Dennis F G Remst, Ellen M W van der Meer-Prins, Yvonne J H de Vaal, Kim H Voogt-Bakker, Rico Buchli, Aiko P J de Vries, Manel Juan, Cynthia S M Kramer, Eduard Palou, Dave L Roelen, Fritz Diekmann, Mirjam H M Heemskerk, Jordi Rovira, Sebastiaan Heidt","doi":"10.1681/ASN.0000001244","DOIUrl":"https://doi.org/10.1681/ASN.0000001244","url":null,"abstract":"<p><strong>Background: </strong>CAR T cell therapy has revolutionized the treatment of hematological malignancies by effectively eliminating tumor cells. In the field of kidney transplantation, comparable cellular therapies are being explored to facilitate transplantation and prevent graft rejection. Chimeric HLA antibody receptor (CHAR) T cells are a promising therapy for eliminating HLA-specific B cells in sensitized patients and potentially ameliorating antibody-mediated rejection. We previously demonstrated that HLA class I CHAR T cells selectively eliminated HLA class I-specific B cells with high specificity. Since HLA sensitization is most often directed against HLA-DQ of the allograft, we developed HLA-DQ2 and HLA-DQ7 CHAR T cells to target B cells with corresponding HLA specificity.</p><p><strong>Methods: </strong>We designed viral vectors encoding HLA-DQ CHARs composed of HLA-DQA1*05:01 alpha chain with either HLA-DQB1*02:01 (HLA-DQ2) or HLA-DQB1*03:01 (HLA-DQ7) beta chains, CLIP peptide, and intracellular 4-1BB costimulatory and CD3ζ signaling domains. Upon production of HLA-DQ CHAR T cells, we evaluated CHAR expression, cytotoxic activity, production of cytokines and cytotoxic mediators, and sensitivity to immunosuppressive drugs in in vitro models. We further assessed the cytotoxic activity of HLA-DQ CHAR T cells in an immunodeficient mouse model and in primary material from sensitized individuals.</p><p><strong>Results: </strong>CHAR-transduced Jurkat Triple Parameter Reporter (JurkatTPR) cells expressing reporter constructs for T cell activation markers showed robust activation upon specific stimulation. Primary CD8+ T cells expressing HLA-DQ2 and HLA-DQ7 CHAR molecules specifically eliminated HLA-DQ2- or HLA-DQ7-specific B cells, respectively, and produced interferon gamma, soluble Fas ligand, perforin, and granzyme B. Maintenance immunosuppressive drug regimens initiated at the time of co-incubation with target cells had limited effects on CHAR T-cell functionality. Finally, HLA-DQ CHAR T cells effectively eliminated HLA-DQ-specific B cells in an in vivo mouse model, as well as in primary material from sensitized individuals.</p><p><strong>Conclusions: </strong>HLA-DQ2 and HLA-DQ7 CHAR T cells, the first HLA class II CHAR T cells, selectively and effectively eliminated corresponding HLA-DQ-specific B cells in vitro, in vivo, and in primary material from sensitized individuals.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887899","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":"Impaired BCAA Catabolism Drives Peritoneal Fibrosis via BCKA-Mediated Suppression of the Pentose Phosphate Pathway.","authors":"Jiayang Li, Tiangang Wu, Junhao Dai, Xin Zhao, Svetlana Reilly, Xin Liu, Dongliang Zhang, Hong Xin, Nan Zhu, Zhiping Li, Zanzhe Yu, Xuemei Zhang","doi":"10.1681/ASN.0000001241","DOIUrl":"https://doi.org/10.1681/ASN.0000001241","url":null,"abstract":"<p><strong>Background: </strong>Peritoneal dialysis (PD) is a life-sustaining therapy for kidney failure, yet its long-term viability is compromised by progressive peritoneal fibrosis in some patients. Currently, reliable treatment options are lacking as the pathogenesis remains poorly understood, with the metabolic underpinnings of fibrotic progression remaining particularly elusive.</p><p><strong>Methods: </strong>Using a physiologically relevant framework comprising human primary mesothelial cells and a PD fluid-exposed mouse model, we performed bidirectional genetic and pharmacological modulation of branched-chain amino acid catabolism. Integrated proteomic and metabolomic analyses were conducted to investigate downstream metabolic consequences.</p><p><strong>Results: </strong>We identified profound impairment in branched-chain amino acid (BCAA) catabolism, centered on a functional bottleneck at the rate-limiting branched-chain α-ketoacid dehydrogenase complex, as a metabolic hallmark of peritoneal fibrosis. Functional uncoupling of the amino acids from their ketoacid derivatives indicated that branched-chain α-ketoacid (BCKA) burden was more closely linked to the fibrotic phenotype than BCAA abundance alone. Mechanistically, BCKA burden was associated with reduced glucose-6-phosphate dehydrogenase expression and activity, lower NADPH-generating capacity, and increased intracellular oxidant burden.</p><p><strong>Conclusions: </strong>Together, these findings showed that BCKA burden, rather than BCAA abundance alone, more closely tracked fibrotic responses and was linked to reduced pentose phosphate pathway-associated redox capacity in peritoneal fibrosis.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":9.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874409","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":"Recurrent Antibiotic-Treated Pyelonephritis Depletes Renal Functional Reserve Despite Preserved Basal GFR in a Reflux-Prone Mouse Model.","authors":"Evan A Rajadhyaksha, Samuel Arregui, Vijay Saxena, Alleé Shaw, Jennifer L Anderson, Sayeh Gholampoor, Gokul Achayaraj, Rose Odom, Danielle E Soranno, David S Hains, Andrew L Schwaderer","doi":"10.1681/ASN.0000001166","DOIUrl":"10.1681/ASN.0000001166","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"2027-2029"},"PeriodicalIF":9.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13567891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148176135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clarifying Crossover Interpretation and Volume-Signal Assessment in ASSIST.","authors":"Dongmei Cheng, Lin Zhan, Huan Zhou","doi":"10.1681/ASN.0000001141","DOIUrl":"10.1681/ASN.0000001141","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":"2079-2080"},"PeriodicalIF":9.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13567889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148205224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}