Kidney international最新文献

{"title":"Optimizing symptom management in people with kidney failure.","authors":"Dharshana Sabanayagam,Chandana Guha,Nicole Scholes-Robertson,Allison Jaure,Germaine Wong","doi":"10.1016/j.kint.2025.07.040","DOIUrl":"https://doi.org/10.1016/j.kint.2025.07.040","url":null,"abstract":"People with kidney failure experience high symptom burden, which is associated with an increased risk of mortality, morbidity, and impaired quality of life. Symptoms are often severe and persistent, affecting many organs and causing considerable physical, psychological and emotional distress. The causes of symptoms are often multifactorial, and the underlying pathophysiology is often poorly understood. Managing symptoms is challenging because of uncertainty regarding the use of validated patient-reported outcome measures in clinical practice and limited evidence for interventions to relieve symptoms. Addressing these challenges requires developing and validating symptom-targeted interventions and integrating symptom management strategies within a multi-disciplinary framework, including nephrologists, palliative care physicians, allied health and mental health professionals. This review provides an overview of the epidemiology, and adverse impacts of symptoms in people with kidney failure. We will also provide practical guidance on selecting the appropriate symptom measures and evidence-based interventions for symptom assessment and management in kidney failure care.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"96 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182651","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":"Mineralocorticoid receptor inhibition in parietal epithelial cells prevents focal segmental glomerulosclerosis and crescentic glomerulonephritis.","authors":"Hélène Lazareth,Olivia Lenoir,Florian Garo,Angélique Rocha,Isabelle Giscos-Douriez,May Fayad,Nasreddine Saidi,Léa Guyonnet,Alexandre Karras,Marcus J Moeller,Carole Hénique-Gréciet,Maria-Christina Zennaro,Sheerazed Boulkroun,Pierre-Louis Tharaux","doi":"10.1016/j.kint.2025.07.037","DOIUrl":"https://doi.org/10.1016/j.kint.2025.07.037","url":null,"abstract":"INTRODUCTIONFocal segmental glomerulosclerosis (FSGS) is a common histological lesion in adults worldwide. It results from initial podocyte injury, followed by a maladaptive activation of glomerular parietal epithelial cells (PEC)s, which leads to progressive scarring of glomeruli. Abnormal PECs phenotype is also a hallmark of crescentic glomerulonephritides, another class of severe kidney diseases that complicate small vessel vasculitides. Current knowledge of the pathophysiological mechanisms leading to PEC activation is limited. Recent evidence indicates an active and destructive role for PECs in extra-capillary glomerular diseases. Therefore, targeting such maladaptive responses could represent a novel therapeutic option to prevent kidney failure in patients. Yet, druggable pathways to prevent or stop the pathogenic behavior of PECs are still elusive.METHODSHere, we examined the role of the mineralocorticoid receptor signaling in PECs in two mouse models of glomerular disease involving PECs activation: a robust model of maladaptive FSGS with deoxycorticosterone acetate (DOCA)-salt administration with uninephrectomy, and nephrotoxic serum-induced crescentic glomerulonephritis.RESULTSWe demonstrate that targeting the mineralocorticoid receptor (MR) (Nr3c2) gene specifically in PECs prevents migration and proliferation after DOCA-salt administration with uninephrectomy. Remarkably, both MR deficiency in PECs and mineralocorticoid receptor pharmacological blockade using eplerenone were also effective in preventing extracapillary lesions and glomerular failure in nephrotoxic serum-induced crescentic glomerulonephritis. Additionally, we revealed a significant overlap between pathways triggered by heparin-binding EGF-like growth factor and its receptor signaling and MR signaling. This promoted the migration, proliferation, and epithelial-to-mesenchymal transition of PECs.CONCLUSIONTogether, our results highlight the common role of MR signaling in the pathophysiology of extra-capillary glomerulopathies, FSGS, and crescentic glomerulonephritis. This supports the use of MR antagonists as potential complementary therapeutic agents with original modes of action for severe diseases.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"1 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153424","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":"Revisiting proliferative glomerulonephritis with monoclonal immunoglobulin deposits through immunoglobulin repertoire sequencing.","authors":"Vincent Javaugue,Virginie Pascal,Samih H Nasr,Sébastien Bender,Paco Derouault,Surendra Dasari,Benjamin J Madden,M Cristine Charlesworth,Lionel Karlin,Céline Lebas,Marc Ulrich,Viviane Gnemmi,Jean-Michel Goujon,Murielle Roussel,Arnaud Jaccard,Nelson Leung,Christophe Sirac,Frank Bridoux","doi":"10.1016/j.kint.2025.07.039","DOIUrl":"https://doi.org/10.1016/j.kint.2025.07.039","url":null,"abstract":"INTRODUCTIONProliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is classified within the spectrum of monoclonal gammopathy of renal significance (MGRS). However, PGNMID features an unexpected low rate of detectable monoclonal gammopathy, questioning the reality of an underlying clonal disorder in most cases.METHODSWe reviewed a cohort of 56 patients with PGNMID focusing on hematological characteristics. To detect discrete underlying clones, we used a highly sensitive high-throughput immunoglobulin (Ig) repertoire sequencing assay from RNA bone marrow (RACE-RepSeq). We also challenged the monoclonality of kidney deposits using immunofluorescence with antibodies specific for light chain (LC) variable region subgroups.RESULTSRACE-RepSeq detected a bone marrow clone corresponding to the deposited Ig in only 23% of the whole cohort. As previously reported, PGNMID-IgG3 was the predominant subtype (41/56, 73%), with an overrepresentation of IgG3 kappa deposits (33/56, 59%). The low prevalence of clonal disorders was driven by PGNMID-IgG3 cases, with only 4/41 (9.8%) patients showing an IgG3-secreting bone marrow clone by RACE-RepSeq. In all seven clone-negative PGNMID-IgG3 kappa cases studied by immunofluorescence with anti-LC variable domain antibodies, glomerular deposits stained for all tested Vκ subgroups, ruling out their monoclonal nature. Compared to control individuals, immunoglobulin repertoire analyses in 24 patients without a detectable clone failed to detect any bias toward the deposited isotype, but showed increased IgG1 representation, suggesting an infectious trigger.CONCLUSIONSOur results suggest that PGNMID is a heterogeneous condition. The predominant subtype most often involves oligoclonal or polyclonal production of nephrotoxic IgG3 and may not derive from a clonal B-cell disorder. Such cases should no longer be classified as MGRS.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"42 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153427","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":"STRATEGIES FOR THE DEVELOPMENT OF SODIUM-GLUCOSE COTRANSPORTER-2 INHIBITORS FOR KIDNEY PROTECTION IN PEDIATRIC CHRONIC KIDNEY DISEASE: PROCEEDINGS OF A WORKSHOP MEETING IN JULY 2023.","authors":"William E Smoyer,Barbara S Gillespie,Louise Oni,Carla Nester,Robert G Nelson,Petter Bjornstad,Hiddo J L Heerspink,Michelle Denburg,Oliver Gross,Jan Marquard,Dominik Steubl,Mark D Lim,Cesia Creighton,Seyi Balogun,Lauren Eva,Kelly Helm,Joshua M Tarnoff,Shamir Tuchman,Mona Khurana,Lily Mulugeta,Lynne Yao,Kirtida Mistry,Aliza Thompson,Howard Trachtman","doi":"10.1016/j.kint.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.kint.2025.09.009","url":null,"abstract":"Pediatric patients with chronic kidney disease (CKD) are treated with nonspecific therapies such as renin-angiotensin-aldosterone system inhibitors; however, there are no approved therapies to slow the progression of pediatric CKD across its diverse etiologies. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated efficacy in slowing the rate of decline in estimated glomerular filtration rate and CKD progression in adults. These therapies hold the promise of similar clinical benefit for pediatric patients with CKD by potentially delaying progression to kidney failure (KF). However, clinical data informing the efficacy, safety, and dosing of these products in pediatric patients with CKD are lacking. To address this issue, a 1.5-day workshop was convened by the Kidney Health Initiative (KHI) and NephCure, with participation from stakeholders that included regulators, National Institutes of Health representatives, trialists, clinicians and investigators, industry representatives, patient advocates, and caregivers. The goal of the workshop was to elucidate the challenges and strategize approaches to evaluate use of SGLT2i in pediatric patients with CKD. To this end, presentations and discussions at the workshop focused on the data supporting the degree to which the course of CKD and expected treatment responses between adult and pediatric populations with CKD are similar, and hence, the degree to which, if any, data from the trials of SGLT2i in adults could be extrapolated to pediatric patients with CKD. Discussions also focused on trial design feasibility, endpoints, gaps in knowledge, and safety considerations for SGLT2i in pediatric CKD. The workshop proposed pathways to advance the evaluation of SGLT2i as therapeutic agents to treat glomerular and non-glomerular pediatric CKD while identifying remaining challenges and research priorities.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"17 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153426","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 kidney slit diaphragm resembles a fishnet.","authors":"Alexandra N Birtasu,Konstantin Wieland,Utz H Ermel,Serena M Arghittu,Sina Manger,Maciej K Kocylowski,Bernd Fakler,Margot P Scheffer,Roberto Covino,Florian Grahammer,Achilleas S Frangakis","doi":"10.1016/j.kint.2025.08.028","DOIUrl":"https://doi.org/10.1016/j.kint.2025.08.028","url":null,"abstract":"INTRODUCTIONAn essential component of the kidney filtration barrier, the slit diaphragm, is a specialized cell-cell junction composed of the cell adhesion molecules Nephrin and Neph1.METHODSHere, we use cryo-electron tomography of vitreous lamellae from high pressure frozen wild type C57BL/6J native mouse glomeruli.RESULTSThe cryo-electron tomograms show that the slit diaphragm resembles a fishnet-like architecture. After sub-tomogram averaging and molecular dynamics flexible fitting of Nephrin and Neph1, the resulting molecular model of the slit diaphragm reveals a cris-cross arrangement of these cell adhesion molecules with multiple homo- and hetero-philic interactions. This renders the slit diaphragm as a single- or a multi-layer fishnet, quasi-crystalline, sheet-like molecular polymer that can provide both stability and flexibility to compensate for mechanical forces.CONCLUSIONThe molecular architecture of the murine slit diaphragm provides a mechanistic framework for comprehending kidney cell-cell junctions with immediate implications in disease.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"42 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153423","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":"Critical role of transcription factor SOX4 in tubular epithelial cell dedifferentiation and fibroblast activation during kidney fibrosis.","authors":"Hao Du,Baihai Jiao,Jian Xing,Dong Yang,Melanie Tran,Penghua Wang,Zhaoyong Hu,Véronique Lefebvre,Dong Zhou,Yanlin Wang","doi":"10.1016/j.kint.2025.08.030","DOIUrl":"https://doi.org/10.1016/j.kint.2025.08.030","url":null,"abstract":"INTRODUCTIONChronic kidney disease (CKD) is a widely prevalent health issue globally. A striking pathological feature of CKD is kidney fibrosis characterized by excessive production and deposition of extracellular matrix (ECM). Tubular epithelial cell (TEC) dedifferentiation and fibroblast activation contribute to the pathogenesis of kidney fibrosis. However, the molecular mechanisms underlying TEC dedifferentiation and fibroblast activation are not fully understood. Here, we investigated the role of SRY-box transcription factor 4 (SOX4) in regulating TEC dedifferentiation and fibroblast activation during the development of CKD.METHODSWe generated global, TEC-specific, and fibroblast-specific SOX4 knockout mice. These mice were subjected to three preclinical models of kidney fibrosis induced by unilateral ureteral obstruction, ischemia-reperfusion injury, or high-dose folic acid to examine the role of SOX4 in TEC dedifferentiation and fibroblast activation during the development of kidney fibrosis. Cultured TECs and fibroblasts were employed to determine the role and molecular mechanisms of SOX4 in regulating TEC dedifferentiation and fibroblast activation in vitro.RESULTSSOX4 was induced in the injured kidneys but its deficiency inhibits TEC dedifferentiation, fibroblast activation and further impeded the development of kidney fibrosis in mice. In vitro, knockdown of SOX4 preserved the epithelial phenotype and inhibited fibroblast activation induced by transforming growth factor-β1 (TGF-β1). Mechanistically, SOX4 facilitated the TGF-β1-Smad3 signaling pathway to promote TEC dedifferentiation and fibroblast activation.CONCLUSIONSOur findings identify SOX4 as a critical factor in TEC dedifferentiation and fibroblast activation suggesting SOX4 may serve as a potential therapeutic target for the treatment of CKD.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"3 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153429","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 single-cell landscape of the human vein after arteriovenous fistula creation and implications for maturation failure.","authors":"Laisel Martinez, Filipe F Stoyell-Conti, Marwan Tabbara, Miguel G Rojas, Simone Pereira-Simon, Nieves Santos Falcon, Reyniel Hernandez Lopez, Daniella Galtes, Christina Kosanovic, Anthony J Griswold, Xiaofeng Yang, Yan-Ting Shiu, Timmy Lee, Juan C Duque, Marco A Ladino, Loay H Salman, Xiaochun Long, Roberto I Vazquez-Padron","doi":"10.1016/j.kint.2025.08.024","DOIUrl":"10.1016/j.kint.2025.08.024","url":null,"abstract":"<p><strong>Introduction: </strong>The biological mechanisms underlying arteriovenous fistula (AVF) maturation in patients receiving hemodialysis remain poorly understood despite decades of research.</p><p><strong>Methods: </strong>To address this gap, we first investigated the cellular changes in the venous wall after fistula creation in histological biopsies of longitudinal veins and AVF samples (23 patients). Using single-cell RNA sequencing of 70,281 cells from independent pre-access veins, early resections, mature, and failed AVFs (20 patients), we then created a complementary transcriptomic atlas of the human vein before and after anastomosis.</p><p><strong>Results: </strong>AVFs had increased wall area and cell number but reduced cell density in histological sections, suggesting that postoperative wall thickening occurs predominantly through extracellular matrix (ECM) deposition. The early remodeling of the AVF was characterized by a loss of smooth muscle cells, increased monocyte infiltration, and the reprograming of myofibroblasts and fibroblasts toward reparative phenotypes. In contrast, later stages of remodeling were dominated by ECM-producing myofibroblasts and fibroblasts, occurring in the context of low cell proliferation. Failed AVFs displayed persistent inflammation and exaggerated healing responses as defining features. Specifically, these AVFs contained abundant proinflammatory and adhesive macrophages with upregulation of the Myddosome signaling complex, proinflammatory vasa vasorum endothelial cells, and hyperactivated fibroblasts and myofibroblasts. Macrophage-derived osteopontin emerged as a key paracrine signal driving vascular cell activation in failed AVFs. Additional signals derived from fibroblasts, myofibroblasts, and endothelial cells, including chemokines, semaphorins, fibroblast growth factors, angiopoietin-like proteins, periostin, and transforming growth factor-β, were also enriched within the inflammatory microenvironment sustaining AVF failure.</p><p><strong>Conclusions: </strong>Our findings uncover previously unrecognized cellular and molecular patterns in human veins following AVF creation, providing novel insights and potential therapeutic targets to improve AVF maturation outcomes.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137688","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 injury and colocalization of complement C3, IgA, and IgG in glomerular immune-complex deposits of patients with IgA nephropathy or IgA vasculitis with nephritis.","authors":"Lea Novak,Stacy D Hall,Gary Cutter,Graham L Gurganus,Dana V Rizk,Bruce A Julian,Mark Haas,Jan Novak","doi":"10.1016/j.kint.2025.07.038","DOIUrl":"https://doi.org/10.1016/j.kint.2025.07.038","url":null,"abstract":"INTRODUCTIONIgA nephropathy (IgAN) and IgA vasculitis-with-nephritis (IgAVN) are considered similar diseases with different spectra of clinical manifestations. Routine immunofluorescence microscopy of kidney-biopsy specimens of patients with IgAN or IgAVN shows glomerular immune-complex deposits with IgA as (co)dominant immunoglobulin and variable staining for IgG. Complement C3 is usually present in both. To assess the relationships of the glomerular immune complexes in IgAN or IgAVN, we determined glomerular C3-IgA, C3-IgG, and IgA-IgG pairwise colocalization and correlated results with severity of kidney injury.METHODSSections of remnant frozen kidney biopsy specimens from patients with IgAN or IgAVN were stained with an IgG Fc specific nanobody and antibodies specific for C3 or IgA. Staining was assessed by high-resolution confocal microscopy. Pairwise colocalization in immune-complex deposits was determined by imaging software and results were correlated with Oxford classification MEST-C scores.RESULTSAll samples had C3, IgA, and IgG in the glomerular immune-complex deposits; predominantly in mesangial areas, with additional peripheral capillary deposits in IgAVN greater than in IgAN. In IgAN, the mean values of the Pearson correlation coefficients were higher for C3-IgA than for C3-IgG or IgA-IgG; in IgAVN they were similar for C3-IgA and IgA-IgG. Furthermore, C3-IgA colocalization was similar in IgAN and IgAVN whereas colocalizations of C3-IgG and IgA-IgG were higher in IgAVN than IgAN. In IgAN, but not IgAVN samples, greater C3-IgA colocalization was significantly associated with individual histologic features of active glomerular injury: mesangial hypercellularity, endocapillary hypercellularity, and cellular/fibrocellular crescents. Analyses using mixed-model repeated measures revealed a trend for the correlation of the sum of M+E+C scores with a higher degree of each pairwise colocalization in IgAN and IgAVN, reaching significance for C3-IgA in IgAN and IgAVN and for C3-IgG in IgAVN.CONCLUSIONSAlthough immune-complex deposits differ between IgAN and IgAVN, our data support the nephritogenic role of C3-IgA-containing immune complexes in both diseases.","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"23 1","pages":""},"PeriodicalIF":19.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145134128","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":"Advances in computational nephropathology.","authors":"David L Hölscher, Roman D Bülow, Martin Strauch, Peter Boor","doi":"10.1016/j.kint.2025.06.029","DOIUrl":"10.1016/j.kint.2025.06.029","url":null,"abstract":"<p><p>Pathology relies on pathologists' qualitative assessment and semiquantitative measures to characterize the structural and molecular alterations of tissues. Novel analytical methods and recent advances in the computational field, particularly in artificial intelligence and deep learning in pathology, termed computational pathology, have led to widespread applications and advancement in research. Integrating computational approaches into the digital pathology workflow can facilitate the automated, high-throughput analysis of histopathologic images, thereby improving precision, reproducibility, and efficiency in pathology diagnostics. We provide a comprehensive overview of the advancements and applications of computational pathology, specifically in nephropathology. We discuss widely adopted methodological approaches, highlighting their respective strengths and limitations, including quantitative nephropathology (i.e., pathomics), deep learning-based image classification and regression, and nonimage applications (e.g., automated decision support systems for standardizing the reporting of current consensus classifications). Despite the promising potential of these approaches, several challenges remain for successful implementation in routine clinical practice. We highlight technological, regulatory, and ethical challenges, such as computational infrastructure, data privacy, and considerations of environmental sustainability. Looking toward the future, we envisage potential developments that could further transform the field. We are entering a new exciting era, where computational methods are reshaping and redefining kidney pathology, perhaps also renaming our field to \"kidnAI\" pathology.</p>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":" ","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113643","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":"Hypertriglyceridemia causing dialysis filter lipid deposition","authors":"William Hartz ,&nbsp;Paul Kinniry","doi":"10.1016/j.kint.2025.04.035","DOIUrl":"10.1016/j.kint.2025.04.035","url":null,"abstract":"","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"108 4","pages":"Page 718"},"PeriodicalIF":12.6,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093497","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}