Frontiers in nephrology最新文献

{"title":"Gd-IgA1-targeting therapy in IgA nephropathy ~what is pathogenic Gd-IgA1?~.","authors":"Kazuaki Mori, Yoshihito Nihei, Yusuke Suzuki","doi":"10.3389/fneph.2026.1977707","DOIUrl":"10.3389/fneph.2026.1977707","url":null,"abstract":"<p><p>IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide, and galactose-deficient IgA1 (Gd-IgA1) is widely recognized as the central pathogenic molecule in the current multi-hit model of IgAN. Over the past few decades, advances in our understanding of IgAN pathogenesis have driven the development of mechanism-based therapies targeting Gd-IgA1-producing cells and the pathways that regulate their differentiation and survival. Recent clinical trials have demonstrated marked reductions in circulating Gd-IgA1, accompanied by significant improvements in proteinuria and preservation of kidney function, highlighting the transition from non-specific disease-modifying therapies toward mechanism-based therapies in IgAN. However, optimizing the use of these emerging therapies requires a deeper understanding of the immune mechanisms responsible for pathogenic Gd-IgA1 production. In this review, we summarize current knowledge regarding the cellular sources and molecular pathways responsible for the production of Gd-IgA1, review recent advances in therapies targeting these cells, and discuss the emerging concept that specific Gd-IgA1 fractions, including IgA-type anti-mesangial cell autoantibodies (IgA-MESCA), may contribute to the disease pathogenesis.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1977707"},"PeriodicalIF":2.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149217506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SGLT2 inhibitors as a strategy for volume management in peritoneal dialysis: a case series.","authors":"R Haridian Sosa Barrios, Miriam Domínguez-Tejedor, Raquel Moreno García, Víctor M Burguera Vion, Milagros Fernández Lucas, Maite E Rivera Gorrín","doi":"10.3389/fneph.2026.1942462","DOIUrl":"https://doi.org/10.3389/fneph.2026.1942462","url":null,"abstract":"<p><p>Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated cardiovascular and renal benefits in chronic kidney disease, yet their role in peritoneal dialysis (PD) remains largely unexplored, and clinical experience is limited. We describe, at the individual-patient level, seven consecutive patients treated with an SGLT2i at a single centre (median age 69 years, range 43-73; five men; one with type 2 diabetes; six dapagliflozin, one empagliflozin). The PD prescription was not modified during treatment, and ultrafiltration refers to the 24-hour drained volume. In the four patients in whom the drug was added to established, unchanged PD, ultrafiltration rose in three and fell in one; the single non-responder was also the only low-average transporter and was later transferred to haemodiafiltration. Both patients anuric at baseline increased their ultrafiltration, and in one of them PD was the only feasible modality. Peritoneal transport category was unchanged wherever paired equilibration tests were available. Serum urate fell in the patients with preserved diuresis but not in those who were anuric, whereas the largest ultrafiltration gain occurred in a patient anuric throughout, dissociating the peritoneal response from any renal effect. The erythropoietin resistance index fell in all treated patients, although the magnitude was clinically relevant in a minority and must be read alongside the haemoglobin trajectory. No patient developed anuria <i>de novo</i>. One patient died of fungal peritonitis in the context of documented non-adherence, an event reported here with its mechanistic implications. These observations support a direct peritoneal mode of action and warrant prospective evaluation with surveillance for fungal infection.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1942462"},"PeriodicalIF":2.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-GBM disease shortly after clinically presumed ANCA-associated vasculitis in an 85-year-old patient: a case report and literature review.","authors":"Hiroki Ito, Hiyu Abe, Yuya Suzuki, Kentaro Yano, Fumiya Sato, Takaki Numahata, Risa Ishikawa, Akari Endo-Matsumoto, Keiji Matsumoto, Tsubasa Yuki, Ayaka Kamada, Hideaki Hashimoto, Go Anan, Katsuya Ishiyama, Takuo Hirose, Takefumi Mori","doi":"10.3389/fneph.2026.1967122","DOIUrl":"10.3389/fneph.2026.1967122","url":null,"abstract":"<p><strong>Introduction: </strong>Sequential emergence of anti-glomerular basement membrane (GBM) disease after anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is rare.</p><p><strong>Case presentation: </strong>An 85-year-old woman presented with fever, edema, elevated myeloperoxidase (MPO)-ANCA, mild urinary abnormalities, markedly elevated urinary tubular injury markers, and negative serum anti-GBM antibodies measured by chemiluminescent enzyme immunoassay. Renal biopsy was not performed because of advanced age, severe dementia, antiplatelet therapy, and the family's preference for non-invasive management. She was clinically presumed to have AAV and achieved apparent clinical remission with prednisolone alone, although MPO-ANCA remained positive. However, 2.5 months after the initial AAV diagnosis, she developed rapidly progressive kidney failure requiring dialysis, accompanied by severe hematuria, increased proteinuria, urinary casts, and markedly elevated anti-GBM antibodies. Clinically diagnosed anti-GBM disease was treated with methylprednisolone pulse therapy, prednisolone, plasma exchange, and hemodialysis. Although renal recovery was not achieved, anti-GBM antibodies became negative, and she remained clinically stable on maintenance hemodialysis for over 4 years while receiving low-dose prednisolone.</p><p><strong>Conclusion: </strong>This case suggests that anti-GBM disease can emerge shortly after apparent clinical remission of AAV. ANCA-mediated GBM injury and age-related GBM changes may contribute to subsequent anti-GBM autoimmunity, although these mechanisms remain hypothetical in this patient. Prompt anti-GBM antibody testing should be considered when a rapid, unexplained decline in kidney function occurs during or after AAV treatment.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1967122"},"PeriodicalIF":2.9,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictors of renal and patient survival in lupus nephritis: a 28-year single-center cohort study.","authors":"Alexandra Vrabie, Bogdan Obrişcă, Bogdan Sorohan, Roxana Jurubiţă, Camelia Achim, Diana Silvia Zilişteanu, Andreea Gabriela Andronesi, Gabriela Lupuşoru, Elena Emanuela Rusu, Raluca Bobeică, Elena Georgia Micu, Sonia Bălănică, Andreea Berechet, Valentin Mocanu, Ştefan Lujinschi, Nicu Caceaune, Gener Ismail","doi":"10.3389/fneph.2026.1945616","DOIUrl":"https://doi.org/10.3389/fneph.2026.1945616","url":null,"abstract":"<p><strong>Introduction: </strong>Despite advances in the understanding and treatment of lupus nephritis (LN), long-term renal and patient outcomes remain suboptimal. Identifying reliable predictors of prognosis and early treatment response is essential for improving risk stratification and guiding management.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of patients with biopsy-proven LN. Long-term renal and patient survival, renal response at 6 and 12 months, and predictors of a composite outcome (doubling of serum creatinine, end-stage kidney disease [ESKD], or death) were evaluated.</p><p><strong>Results: </strong>A total of 147 patients were included, with a median follow-up of 39.5 months. 10.3% of patients had a doubling of serum creatinine, 11.0% progressed to ESKD, and 6.8% died. Proteinuria <0.7 g/day was achieved by 49.1% and 54.4% of patients at 6 and 12 months, respectively. In multivariate analysis, baseline predictors of the composite outcome included age >50 years, proteinuria ≥3 g/day, and hemoglobin <10 g/dL, while an activity index ≥9 and low baseline C4 levels showed a protective trend. Achieving proteinuria <0.7 g/day at 12 months emerged as the strongest protective factor. A prognostic score demonstrated good discrimination (area under the curve [AUC] 0.82), which improved further with the addition of proteinuria at 12 months (AUC 0.86).</p><p><strong>Conclusions: </strong>In this biopsy-proven LN cohort, early renal response, particularly proteinuria <0.7 g/day at 12 months, was the strongest predictor of long-term renal and patient survival. These findings support a dynamic, response-based approach to prognostication in LN and provide the basis for a clinically applicable prognostic score that requires external validation.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1945616"},"PeriodicalIF":2.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-transplant ureteral stenosis: donor-related risk factors, graft outcome and surgical management.","authors":"T Wagner, Hauke Heinrich, E Schober, L Ischebeck, N Schleussner, M Hummels, F C Koehler, C Kurschat, M Kann, C Bruns, D L Stippel, M N Thomas","doi":"10.3389/fneph.2026.1943229","DOIUrl":"10.3389/fneph.2026.1943229","url":null,"abstract":"<p><strong>Introduction: </strong>Kidney transplantation remains the preferred treatment for end-stage renal disease; however, the increasing use of extended-criteria donors has been associated with a higher incidence of postoperative complications.</p><p><strong>Methods: </strong>We retrospectively analyzed 471 kidney transplant recipients at the University of Cologne between 2012 and 2022 to evaluate the incidence, risk factors, clinical outcomes, and surgical management of ureteral stenosis.</p><p><strong>Results: </strong>Ureteral stenosis occurred in 6.37% and was significantly associated with older donor age within the extended-criteria donor range (65 vs. 56 years, p = 0.006), multiple renal arteries (33.3% vs. 10.2%, p < 0.001), and BK virus infection, as reflected by higher rates of BK viruria (26.7% vs. 7.0%, p = 0.002) and BK viraemia (26.7% vs. 8.6%, p = 0.005). Renal function was significantly impaired in recipients with ureteral stenosis at 6 months, 1 year, and 2 years after transplantation. Death-censored graft survival was significantly lower in the stenosis group (79.7% vs. 93.3%, p = 0.01).</p><p><strong>Discussion: </strong>Ureteral transposition and ureteroneocystostomy demonstrated comparable outcomes, long-term renal function and graft survival supporting individualization of surgical technique based on anatomical and patient-specific factors.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1943229"},"PeriodicalIF":2.9,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complement biomarkers in IgA nephropathy: current insights and clinical relevance.","authors":"Altynay Balmukhanova, Chee Eng Chan, Jonathan Barratt","doi":"10.3389/fneph.2026.1918450","DOIUrl":"10.3389/fneph.2026.1918450","url":null,"abstract":"<p><p>IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and is a major contributor to the global burden of chronic kidney disease. Strong evidence highlights complement activation as a key driver of the disease pathogenesis and its progression. In this regard, the emergence of new therapies targeting the complement system has further increased interest in specific biomarkers that can help in diagnosis, prognosis, and assessment of response to therapy in patients with IgAN. Although complement biomarkers show promising associations with disease severity and prognosis, most remain exploratory and lack adequate validation for routine clinical application. Further research should focus on standardization and prospective multicenter validation of putative biomarkers to facilitate a biomarker-driven approach to the use of complement inhibitors in IgAN. Therefore, this review summarizes a growing body of evidence on the role of complement-related biomarkers in IgAN and discusses their diagnostic and prognostic potential, as well as several limitations for implementation in clinical practice.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1918450"},"PeriodicalIF":2.9,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The lactate dehydrogenase-to-albumin ratio is independently associated with moderate-to-severe tubulointerstitial fibrosis in patients with IgA nephropathy.","authors":"Luli Zheng, Guokai Yang","doi":"10.3389/fneph.2026.1931478","DOIUrl":"https://doi.org/10.3389/fneph.2026.1931478","url":null,"abstract":"<p><strong>Background: </strong>Tubulointerstitial fibrosis accelerates the progression of immunoglobulin A nephropathy (IgAN) to end-stage renal disease (ESRD). While renal biopsy is the standard for evaluation, non-invasive biomarkers remain scarce. This study investigated the independent association and diagnostic value of the lactate dehydrogenase-to-albumin ratio (LAR) for moderate-to-severe tubulointerstitial fibrosis (Oxford T1+T2) in IgAN patients.</p><p><strong>Methods: </strong>We retrospectively analyzed 398 patients with biopsy-proven primary IgAN, categorized into no/mild fibrosis (T0, n=273) and moderate-to-severe fibrosis (T1+T2, n=125) groups. Clinical, laboratory, and pathological data were collected to calculate LAR. Missing data were handled using multiple imputation by chained equations (MICE). Statistical evaluations included logistic regression, ROC curves, restricted cubic splines (RCS), and subgroup analyses.</p><p><strong>Results: </strong>The T1+T2 group exhibited significantly higher median LAR levels (5.10 vs. 4.13, P < 0.001). Following adjustment for confounders, LAR remained independently associated with fibrosis (OR = 1.425, 95% CI: 1.122-1.809, P = 0.004). The AUC was 0.717, with an optimal cut-off of 4.91 (sensitivity 56.8%, specificity 78.0%). RCS analysis indicated a linear relationship (P for non-linearity = 0.2350). Subgroup analyses showed consistent positive associations (OR > 1.2), reaching statistical significance in males, patients aged ≥40 years, and those with eGFR ≥60 mL/min/1.73 m². Sensitivity analyses confirmed robustness. Patients with LAR > 4.91 demonstrated worse renal function, heavier proteinuria, and higher fibrosis incidence (54.2% vs. 20.2%, P < 0.001).</p><p><strong>Conclusion: </strong>LAR is independently associated with moderate-to-severe tubulointerstitial fibrosis and demonstrates moderate diagnostic efficacy. As a cost-effective indicator, LAR may serve as a non-invasive auxiliary tool for clinical screening and risk stratification in IgAN, but it cannot replace renal biopsy as the diagnostic gold standard.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1931478"},"PeriodicalIF":2.9,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13635296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Advancement in kidney care: targeted delivery and precision medicine approaches.","authors":"Domenico Cerullo, Sonia Fiori, Manuel Alfredo Podestà","doi":"10.3389/fneph.2026.1977844","DOIUrl":"https://doi.org/10.3389/fneph.2026.1977844","url":null,"abstract":"","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1977844"},"PeriodicalIF":2.9,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13630749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond renal support: biological modulation across pathophysiological domains during continuous renal replacement therapy - a randomized pilot study.","authors":"Fernando Sánchez-Morán, Salvador Pérez, Juan Sastre-Belloch, María Lidón Mateu-Campos","doi":"10.3389/fneph.2026.1932419","DOIUrl":"10.3389/fneph.2026.1932419","url":null,"abstract":"<p><strong>Background: </strong>Continuous renal replacement therapy (CRRT) is the preferred extracorporeal renal support modality for haemodynamically unstable critically ill patients with acute kidney injury (AKI). Although regional citrate anticoagulation (RCA) is primarily used to maintain circuit patency, its biological effects may extend beyond anticoagulation itself. We hypothesized that different anticoagulation strategies are associated with distinct biological modulation across complementary pathophysiological domains during CRRT.</p><p><strong>Methods: </strong>We conducted a prospective randomized pilot trial comparing RCA with systemic unfractionated heparin in critically ill adults with AKI requiring CRRT (1:1 allocation). Serial blood samples were obtained before CRRT initiation, at 1 hour and at 24 hours, with paired pre- and post-filter sampling at 1 and 24 hours. Biomarkers represented redox homeostasis (glutathione -GSH, GSSG- and their ratio), neutrophil activation (myeloperoxidase -MPO-), cellular injury (cell-free DNA -cfDNA-) and systemic inflammation (C-reactive protein -CRP-). Healthy reference participants established physiological reference values. Longitudinal analyses used linear mixed-effects models with fixed effects for time, anticoagulation strategy and their interaction. This trial was registered in the European Clinical Trials Database (EudraCT No. 2016-004361-12) and at ClinicalTrials.gov (NCT06646328).</p><p><strong>Results: </strong>Twenty patients were randomized equally to RCA or systemic heparin; baseline characteristics were comparable between groups. Among six biomarkers spanning four pathophysiological domains, only MPO showed a significant systemic time × anticoagulation interaction (P = .008); although baseline-adjusted sensitivity analyses did not confirm a significant between-group difference. GSH and cfDNA changed significantly over time irrespective of anticoagulation strategy (both P = .016), while the GSSG/GSH ratio approached a treatment-level difference (P = .067). Across the extracorporeal circuit, CRP increased significantly post-filter at both timepoints, MPO increased at 1h, and GSH showed an anticoagulation-dependent pre-to-post change at 1h. No significant differences were observed in secondary clinical outcomes.</p><p><strong>Conclusions: </strong>These pilot findings suggest that different anticoagulation strategies during CRRT may show domain-specific, rather than uniform, biological modulation, most evident within the neutrophil activation domain, with additional evidence of biomarker-specific kinetics across the extracorporeal circuit. These exploratory results are compatible with the concept that extracorporeal therapies may influence distinct domains differently, a hypothesis warranting confirmation in adequately powered, prospectively designed studies before implications for precision extracorporeal therapy can be drawn.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1932419"},"PeriodicalIF":2.9,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13643268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvement in peritoneal dialysis exit-site infection rates in an integrated health care system in the United States.","authors":"Max T Hukill, Andrea M Yeung, Talha H Imam","doi":"10.3389/fneph.2026.1825353","DOIUrl":"https://doi.org/10.3389/fneph.2026.1825353","url":null,"abstract":"<p><strong>Introduction: </strong>Exit-site infections (ESIs) are a significant complication of peritoneal dialysis (PD) due to their potential to progress to peritonitis, leading to higher rates of morbidity, mortality, and PD dropout. ESI rates and trends have not been generally recorded or reported by established registries. To address this gap, we studied data from ten Kaiser Permanente Southern California (KPSC) hospitals over the last decade to report yearly PD ESI rates and examine trends over time.</p><p><strong>Methods: </strong>This is a historical cohort study using data provided by the Renal Registry of Southern California Permanente Medical Group (SCPMG) for ten KPSC hospitals. Each hospital provided quarterly data from 2014-2023 with number of patients and ESI rate, reported as episodes per 100 patient-months. We modeled quarterly ESI rates across all centers (2014-2023) using a Tweedie generalized linear mixed model with calendar year and program size as fixed effects, accounting for repeated measures within center.</p><p><strong>Results: </strong>The overall mean ESI rate across the study period was 0.86 episodes per 100 patient-months (95% CI: 0.68-1.05). The observed mean ESI rate was 1.26 (95% CI: 0.98-1.60) episodes per 100 patient-months in 2014, compared with 0.72 (95% CI: 0.42-1.07) in 2023. Each additional calendar year was associated with a 6.4% relative decrease in ESI rate (rate ratio [RR] 0.94, 95% CI 0.89-0.99, <i>p</i> = 0.011), corresponding to an estimated 45.1% decline in ESI rate over the study period (95% CI: 12.8-65.4%). Program size was not significantly associated with ESI rate after adjustment for calendar year (RR 0.76 per 100-patient increase, 95% CI 0.52-1.11, <i>p</i> = 0.15).</p><p><strong>Conclusion: </strong>We found a significant decline in ESI rates across ten KPSC hospitals from 2014 to 2023. This decline was not explained by growth in program size, suggesting that other factors-such as evolving infection prevention practices, staff training, or care coordination-may have contributed, though our data do not permit us to test these mechanisms directly. We encourage prospective or mechanism-specific studies to explore which factors are driving these improvements.</p>","PeriodicalId":73091,"journal":{"name":"Frontiers in nephrology","volume":"6 ","pages":"1825353"},"PeriodicalIF":2.9,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13626983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}