Kidney International Reports最新文献

{"title":"Kidney Damage in a Post–Hematopoietic Stem Cell Transplantation Patient With Dense Deposit Disease and Thrombotic Microangiopathy–Like Changes","authors":"Lijun Wang , Zhihuang Zheng , Yijue Song , Yu Cai , Liping Wan , Qing Yu , Jinfang Bao , Jun Liu","doi":"10.1016/j.ekir.2025.06.005","DOIUrl":"10.1016/j.ekir.2025.06.005","url":null,"abstract":"","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 3284-3287"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Desmopressin After Kidney Biopsy: Are the Risks Worth it?","authors":"Taha Enes Cetin , Ozant Helvaci","doi":"10.1016/j.ekir.2025.06.058","DOIUrl":"10.1016/j.ekir.2025.06.058","url":null,"abstract":"","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Page 3292"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Nucleus RNA-Sequencing Identifies a Differential Profibrotic Response in Parietal Epithelial Cells in Primary Versus Maladaptive Focal Segmental Glomerulosclerosis","authors":"Dries Deleersnijder ,&nbsp;Tom Venken ,&nbsp;Rogier Schepers ,&nbsp;Thomas Van Brussel ,&nbsp;Björn K. Meijers ,&nbsp;Ben Sprangers ,&nbsp;Diether Lambrechts ,&nbsp;Amaryllis H. Van Craenenbroeck","doi":"10.1016/j.ekir.2025.06.023","DOIUrl":"10.1016/j.ekir.2025.06.023","url":null,"abstract":"<div><h3>Introduction</h3><div>Focal segmental glomerulosclerosis (FSGS) lesions occur in a wide range of clinical conditions that are all characterized by critical podocyte injury. Differentiating primary from maladaptive forms of FSGS remains challenging because of the absence of reliable biomarkers, resulting from a lack of insight into their pathophysiological differences.</div></div><div><h3>Methods</h3><div>We used single-nucleus RNA-sequencing (snRNA-seq) to identify differentially expressed transcriptional signatures in kidney biopsies of well-phenotyped primary versus maladaptive FSGS. We included cryopreserved kidney biopsy cores from adult patients with newly diagnosed primary FSGS (<em>n</em> = 9, all nephrotic), maladaptive FSGS (<em>n</em> = 9, all nonnephrotic), proteinuric controls (antiphospholipase A2 receptor antibody–positive membranous nephropathy [PLA2R+ MN], <em>n</em> = 3), and healthy controls (<em>n</em> = 4).</div></div><div><h3>Results</h3><div>We identified 120,751 high-quality nuclei, including 2471 podocytes and 1574 parietal epithelial cells (PECs). In primary FSGS, podocytes showed a more pronounced but not specific injury pattern with upregulation of immune pathways, such as antigen presentation, and mammalian target of rapamycin (mTOR) complex 1 (mTORC1)-signaling. Glomerular cell-cell interaction analysis showed increased profibrotic TGF-β and PDGFR-β signaling in primary FSGS PECs, which also upregulated genes that compose the normal PEC-derived extracellular matrix (ECM) (<em>LAMB1, COL4A1, COL4A5, COL4A6</em>). In maladaptive FSGS, podocytes showed few differentially expressed genes (DEGs) and PEC-PEC interactions predominated. Here, a (myo-)fibroblast-like PEC subpopulation upregulated non–type IV fibril- and network-forming collagens (<em>COL1A1, COL5A1, COL8A1</em>), which may further contribute to the development of glomerulosclerosis.</div></div><div><h3>Conclusion</h3><div>This study presents a single-cell transcriptional landscape of well-phenotyped patients with FSGS and provides evidence for a differential profibrotic PEC response in primary versus maladaptive FSGS.</div></div>","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 3255-3270"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overcoming Diagnostic Disparities in Kidney Disease: A Call to Action","authors":"Mythri Shankar ,&nbsp;Becky Mingyao Ma ,&nbsp;Marek Kollar ,&nbsp;Ana Catalina Alvarez-Elias ,&nbsp;Carmen Elena Cervantes ,&nbsp;Chimezie Godswill Okwuonu ,&nbsp;Priti Meena ,&nbsp;Rasha Hussein ,&nbsp;Tae Won Yi ,&nbsp;Yogeshni Chandra ,&nbsp;Vivekanand Jha ,&nbsp;Daniel Vincent O’Hara ,&nbsp;ISN - Emerging Leaders Program Cohort 3","doi":"10.1016/j.ekir.2025.07.002","DOIUrl":"10.1016/j.ekir.2025.07.002","url":null,"abstract":"","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 2901-2904"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steroid Avoidance in Kidney Transplantation: From Vision to Velocity","authors":"Krishnam Raju Penmatsa ,&nbsp;Ankur Gupta","doi":"10.1016/j.ekir.2025.07.016","DOIUrl":"10.1016/j.ekir.2025.07.016","url":null,"abstract":"","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 2905-2906"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Body Speaks Louder Than the Belly: Systemic Inflammation Drives Peritoneal Dialysis Outcomes","authors":"Roberto Pecoits-Filho ,&nbsp;Elba Medina","doi":"10.1016/j.ekir.2025.06.051","DOIUrl":"10.1016/j.ekir.2025.06.051","url":null,"abstract":"","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 2907-2908"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144934104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monitoring Sodium Intake With a Salt Meter in Hemodialysis Patients","authors":"Wilaiporn Akkabut ,&nbsp;Wasan Trakulsuntornchai ,&nbsp;Sutasiny Junhoaton ,&nbsp;Rungthiwa Kitpermkiat ,&nbsp;Prapimporn Chattranukulchai Shantavasinkul ,&nbsp;Surasak Kantachuvesiri","doi":"10.1016/j.ekir.2025.06.027","DOIUrl":"10.1016/j.ekir.2025.06.027","url":null,"abstract":"<div><h3>Introduction</h3><div>Patients on hemodialysis experience a progressive inability to regulate sodium and water balance as kidney function declines. This study investigated the potential of self-monitoring of sodium intake using a salt meter and intensive dietary education in patients on hemodialysis.</div></div><div><h3>Methods</h3><div>This feasibility, quasi-experimental study recruited patients on hemodialysis from 2 hemodialysis units; the units as a whole were assigned to receive intensive dietary education in combination with a dietary diary and salt meter for 8 weeks (intervention group) or standard dietary education alone (control group). Blood pressure (BP) and sodium-related outcomes were measured at baseline, and at 8 and 16 weeks.</div></div><div><h3>Results</h3><div>We analyzed 21 patients in the intervention group and 25 in the control group. Mean interdialytic weight gain (IDWG) remained stable in the intervention group but increased in the control group from baseline by 0.9 and 1.2 kg (at week 8 and 16, respectively). The mean systolic BP decreased by 9.7 mm Hg from baseline to week 16 in the intervention group and increased by 10.7 and 13.7 mm Hg (at week 8 and 16, respectively) in the control group (<em>P</em> &lt; 0.05). Serum sodium levels in the intervention group decreased significantly from baseline by 1.8 mmol/l at 8 weeks (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Intensive dietary education combined with salt meter–based self-monitoring of sodium intake was more effective than standard education alone in controlling serum sodium and BP with improved adherence to the low-salt diet. Salt meters may be useful to support sodium restriction in patients on hemodialysis.</div></div>","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 3081-3093"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular Complications in ADPKD","authors":"Niloufar Ebrahimi ,&nbsp;Yasar Caliskan ,&nbsp;Pranav S. Garimella ,&nbsp;Sol Carriazo ,&nbsp;Fouad T. Chebib ,&nbsp;Giv Heidari Bateni ,&nbsp;Neera K. Dahl ,&nbsp;Anjay Rastogi ,&nbsp;Amir Abdipour ,&nbsp;Sayna Norouzi","doi":"10.1016/j.ekir.2025.06.054","DOIUrl":"10.1016/j.ekir.2025.06.054","url":null,"abstract":"<div><div>Autosomal dominant polycystic kidney disease (ADPKD), primarily caused by mutations in the <em>PKD1</em> or <em>PKD2</em> gene, is among the most common hereditary kidney diseases worldwide and is associated with significant extrarenal manifestations, including cardiovascular disease. In patients with ADPKD, cardiovascular disease is the major cause of mortality and is associated with a high burden of comorbidities. Cardiovascular manifestations include hypertension, which may lead to left ventricular hypertrophy (LVH) and diastolic dysfunction, as well as valvular abnormalities, aortic aneurysm, and pericardial effusion (PCE). The cardiovascular manifestations can present early as part of the ADPKD manifestation or later because of chronic kidney disease (CKD) progression. Early detection of cardiovascular manifestations can play a pivotal role in better management of these patients. Hypertension in ADPKD might start at an early age and is driven by a complex interplay of polycystin (PC) dysfunction, intracellular signaling disruptions, and activation of the renin-angiotensin-aldosterone system (RAAS), which can contribute to vascular structural changes and impaired endothelial function. Valvular involvement exhibits a bimodal pattern of age distribution, with early manifestations occurring in younger patients likely linked to genetic factors and later complications emerging as part of CKD progression. This review explores cardiovascular complications in ADPKD, emphasizing the need for early detection, and briefly provides an overview of tailored management approaches to improve outcomes in this high-risk population.</div></div>","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 2953-2966"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lower Podocyte Number per Glomerulus Associates With Progressive CKD","authors":"Aleksandar Denic ,&nbsp;Afsana A. Shaik ,&nbsp;Syed Khooshal Fareeduddin ,&nbsp;Aperna Fnu ,&nbsp;Mahesh Kumar ,&nbsp;Aidan F. Mullan ,&nbsp;Vidit Sharma ,&nbsp;Mariam P. Alexander ,&nbsp;Akhilesh Pandey ,&nbsp;Roger C. Wiggins ,&nbsp;Jeffrey B. Hodgin ,&nbsp;Stuart J. Shankland ,&nbsp;Andrew D. Rule","doi":"10.1016/j.ekir.2025.06.004","DOIUrl":"10.1016/j.ekir.2025.06.004","url":null,"abstract":"<div><h3>Introduction</h3><div>Podocyte depletion may play an important role in chronic kidney disease (CKD); however, longitudinal clinical studies are lacking in populations without obesity-related glomerulopathy.</div></div><div><h3>Methods</h3><div>Patients studied underwent radical nephrectomy for tumors between 2000 and 2021 and had &lt; 10% interstitial fibrosis and tubular atrophy (IFTA) on histology. Cases who developed progressive CKD were identified by the onset of dialysis, kidney transplantation, sustained estimated glomerular filtration rate (eGFR) &lt; 10 ml/min per 1.73 m², or sustained 30% eGFR decline after the postnephrectomy baseline eGFR. Each case of progressive CKD was age-sex-matched to a control without progressive CKD at the same follow-up time. Podometric measures (number/glomerulus, density, and cell volume) and parietal epithelial cell (PEC) measures (number/glomerulus and density) were determined with immunohistochemistry and stereology. The risk of progressive CKD with podometric measures was assessed, adjusting for glomerular tuft volume, glomerulosclerosis, IFTA, and arteriosclerosis (all determined by morphometry) or adjusting for age, sex, diabetes mellitus, body mass index (BMI), hypertension, eGFR, and proteinuria.</div></div><div><h3>Results</h3><div>There were 35 CKD cases and 35 controls studied. Cases versus controls did not differ significantly by BMI (mean: 29.1 vs. 28.2 kg/m², <em>P</em> = 0.88), glomerular tuft volume, or PEC number, but had lower podocyte number, lower podocyte density, and lower PEC density. Lower podocyte number correlated with several nephrosclerosis measures. In adjusted analyses, podocyte number and podocyte density associated with progressive CKD and these associations did not substantively differ by cortex depth.</div></div><div><h3>Conclusion</h3><div>Low podocyte number per glomerulus is associated with the development of progressive CKD independent of CKD risk factors, kidney function, glomerular volume, and nephrosclerosis severity.</div></div>","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 3213-3224"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defining Relationships Among Tests for Kidney Transplant Antibody-Mediated Rejection","authors":"Katelynn S. Madill-Thomsen ,&nbsp;Luis G. Hidalgo ,&nbsp;Zachary P. Demko ,&nbsp;Philippe M. Gauthier ,&nbsp;Adam Prewett ,&nbsp;Dave Lowe ,&nbsp;Jessica J. Chang ,&nbsp;Martina Mackova ,&nbsp;Klemens Budde ,&nbsp;Jonathan S. Bromberg ,&nbsp;Philip F. Halloran","doi":"10.1016/j.ekir.2025.06.017","DOIUrl":"10.1016/j.ekir.2025.06.017","url":null,"abstract":"<div><h3>Introduction</h3><div>Effective therapies for kidney transplant antibody-mediated rejection (ABMR) will require accurate diagnoses plus assessment of ABMR activity, and the new tests that were used to show treatment effects in the clinical trial such as donor-derived cell-free DNA (dd-cfDNA) and molecular biopsy analysis (the Molecular Microscope Diagnostic System) could be useful.</div></div><div><h3>Methods</h3><div>Trifecta-Kidney (<span><span>ClinicalTrials.gov</span><svg><path></path></svg></span> #NCT04239703) studied 717 indication biopsies to define the relationships among the following 4 tests used for ABMR: (i) standard-of-care (SOC) local histologic biopsy ABMR diagnosis, (ii) MMDx ABMR diagnosis, (iii) dd-cfDNA, and (iv) donor-specific antibody (DSA).</div></div><div><h3>Results</h3><div>All 4 tests were correlated in a partial correlation network, with a hierarchy of intertest correlations: MMDx ABMR &gt; dd-cfDNA &gt; histology ABMR &gt; DSA. Surprisingly, DSA correlated at least as strongly with MMDx ABMR as with histologic ABMR, even though DSA is not used in MMDx. When expressed in the same 6 rejection classes, MMDx diagnosed ABMR more frequently than histology. When histology disagreed with MMDx ABMR, dd-cfDNA and DSA correlated more strongly with MMDx assessment. However, histology also detected ABMR lesions in some cases that MMDx called No Rejection, correlating with subthreshold molecular ABMR activity, dd-cfDNA and DSA (AJT 25:72-87, 2024). Molecular rejection predicted graft outcomes better than histologic rejection in Trifecta-Kidney, and this finding was confirmed in the earlier INTERCOMEX study cohort.</div></div><div><h3>Discussion</h3><div>The 4-way intertest correlations extend below current thresholds for diagnosing ABMR. These results map a network of 4 ABMR-related tests that can add precision to ABMR assessment in trials and clinical management, and highlight the need to establish the clinical significance of subthreshold ABMR activity.</div></div>","PeriodicalId":17761,"journal":{"name":"Kidney International Reports","volume":"10 9","pages":"Pages 3225-3238"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}