Nephrology (Carlton, Vic.)最新文献

{"title":"Evaluation of a Chronic Kidney Disease e-Phenotype: Identification and Characterisation by Electronic Health Record Data.","authors":"Christopher Sparks, Adam G Steinberg, Timothy Fazio, Geva Hilzenrat, Brett Sobey, Nigel D Toussaint","doi":"10.1111/nep.70248","DOIUrl":"10.1111/nep.70248","url":null,"abstract":"<p><strong>Aim: </strong>Develop and evaluate a chronic kidney disease (CKD) electronic (e-) phenotype to identify and risk-stratify CKD patients at scale using electronic health record (EHR) data.</p><p><strong>Methods: </strong>Patient encounter and laboratory data determining kidney function and proteinuria from a four-year period (2021-2024) at a large Australian tertiary referral hospital was extracted from the hospital EHR. Following exclusion of kidney transplant recipients and patients on dialysis, eligible patients were classified as having CKD based on ICD-10 codes, decreased estimated glomerular filtration rate (eGFR, < 60 mL/min per 1.73 m²) and/or albuminuria (urine albumin-to-creatinine ratio [uACR] ≥ 3 mg/mmol, A2/A3 equivalent) for a minimum of 3 months. Patients with sufficient laboratory data were also staged according to the Kidney Disease Improving Global Outcomes (KDIGO) A-by-G grid.</p><p><strong>Results: </strong>From a total undifferentiated hospital cohort of n = 342 146, the CKD e-phenotype algorithm identified n = 17 908 likely CKD cases (5.2%). Algorithm-detected CKD cases were validated against blinded manual chart review (n = 200), revealing sensitivity and specificity for CKD by ICD-10 codes (0.85 and 0.83), eGFR (0.62 and 0.98) and proteinuria criteria (0.33 and 0.75). The proportion of patients that were ICD-10-coded for CKD increased significantly (p < 0.001) with increasing G-stage (odds ratio [OR] 3.05) and A-stage (OR 2.31).</p><p><strong>Conclusion: </strong>Incorporating eGFR and proteinuria data into the e-phenotype algorithm appears to identify novel CKD cases with high specificity, particularly in the earlier stages of CKD progression. However, overall sensitivity is limited when compared to ICD-10 CKD codes alone.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 8","pages":"e70248"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148582049","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":"Comment on \"Self-Reported Sleep Duration, Death-Censored Graft Failure and Health-Related Quality of Life Among Kidney Transplant Recipients: Results From the KNOW-KT Study\".","authors":"Sachin Kumar, Nirupma Gupta, Sujeet Kumar Singh, Hariharan Srinivasan, Varshini Vadhithala, Sushma Narsing Katkuri, Brajgopal Kushwaha","doi":"10.1111/nep.70266","DOIUrl":"10.1111/nep.70266","url":null,"abstract":"","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 8","pages":"e70266"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13477839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761500","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":"Persistent Haematuria Is Associated With Reduced Kidney Survival in Primary Podocytopathies.","authors":"Gabriel Ștefan, Nicoleta Petre, Adrian Zugravu, Simona Stancu","doi":"10.1111/nep.70252","DOIUrl":"10.1111/nep.70252","url":null,"abstract":"<p><strong>Aim: </strong>Haematuria is frequently present in podocytopathies, but its significance and prognostic value are not well described. This study aimed to determine the prevalence and association between persistent haematuria and kidney survival in patients with membranous nephropathy (MN), minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS).</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of 236 adults with biopsy-proven primary podocytopathies. Persistent haematuria was defined as ≥ 5 red blood cells per high-power field in ≥ 3 consecutive urine specimens within 3 months post-biopsy. The primary outcome was end-stage kidney disease (ESKD) requiring chronic renal replacement therapy. Kaplan-Meier analysis and Cox proportional hazards regression were performed.</p><p><strong>Results: </strong>Among 236 participants (114 MN, 76 MCD, 46 FSGS), 73 (31%) had persistent haematuria. Participants with haematuria had higher proteinuria (5.3 vs. 3.2 g/g, p = 0.01) and were more likely to have hypertension (55% vs. 36%, p = 0.007). During a median follow-up of 96 months, 38 patients (16%) reached ESKD. ESKD incidence was significantly higher in patients with persistent haematuria (32% vs. 9%, p < 0.001). After adjusting for diagnosis, eGFR, proteinuria, Charlson comorbidity score and histological chronicity score, persistent haematuria remained independently associated with ESKD (hazard ratio: 3.55; 95% CI: 1.78-7.05; p < 0.001).</p><p><strong>Conclusion: </strong>Persistent haematuria is prevalent among patients with podocytopathies and is significantly and independently associated with ESKD. Urinalysis, including microscopic haematuria assessment, is widely available and inexpensive, providing a valuable data point to help formulate patient prognosis.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 8","pages":"e70252"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148665519","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":"CD4- and CD8-to-Total Lymphocyte Ratios to Guide Rabbit Anti-Thymocyte Globulin Induction in Kidney Transplant Recipients: A Single-Center Feasibility Study.","authors":"I-Ru Chen, Ping-Chin Lai, Chiu-Ching Huang, Huey-Liang Kuo, Chang-Cheng Jiang, Chia-Hui Chou, Chao-Hsiang Chang, Chi-Ping Huang, Chin-Chung Yeh, Po-Jen Hsiao, Guan-Heng Chen, Yu-Cyuan Hong, Yi-Huei Chang","doi":"10.1111/nep.70267","DOIUrl":"10.1111/nep.70267","url":null,"abstract":"<p><strong>Aim: </strong>Rabbit anti-thymocyte globulin (rATG) is widely used for induction immunosuppression in kidney transplantation, but conventional dosing is largely weight based and may not reflect dynamic interindividual immune responses. We aimed to evaluate a predefined, individualized dosing strategy guided by peripheral CD4-to-total lymphocyte (CD4/TLC) and CD8-to-total lymphocyte (CD8/TLC) ratios and to assess its feasibility and 1-year outcomes.</p><p><strong>Methods: </strong>In this single-center retrospective cohort study conducted in Taiwan from 2018 to 2024, 76 adult kidney transplant recipients received rATG titrated by serial flow cytometry to a predefined target of both CD4/TLC and CD8/TLC ratios < 10%. We evaluated cumulative rATG exposure, lymphocyte-subset response, for-cause biopsy-proven acute rejection (BPAR), graft function, graft loss, hospitalization-requiring infections, and mortality over 1 year.</p><p><strong>Results: </strong>The median cumulative rATG dose was 1.2 mg/kg (IQR, 1.1-1.5; maximum, 3.8). Thirty-eight recipients (50.0%) reached the immunologic target after a single intraoperative dose (1-1.5 mg/kg). At 1 year, for-cause BPAR occurred in 1 recipient (1.3%), mean serum creatinine was 1.20 mg/dL, and no graft loss occurred. Seventeen recipients experienced hospitalization-requiring infections, accounting for 22 episodes. No CMV disease or biopsy-proven BK virus nephropathy was observed. Four recipients (5.3%) died, including two deaths related to opportunistic fungal infections.</p><p><strong>Conclusion: </strong>CD4/TLC- and CD8/TLC-guided rATG dosing was feasible and achieved predefined immunologic targets with low cumulative rATG exposure in this cohort. These findings support prospective controlled studies to evaluate the clinical utility, safety, and comparative effectiveness of this individualized dosing strategy.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 8","pages":"e70267"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13457984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148709388","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":"miR-145-5p Targets KLF4 to Regulate the SIRT3/GPX4 Axis, Mediating Ferroptosis and Exacerbating Tubular Epithelial Cell Injury in Diabetic Nephropathy.","authors":"Hongjin Tan, Zuopeng Lu, Meirong Xu, Ganlin Wu, Yu Cao","doi":"10.1111/nep.70237","DOIUrl":"10.1111/nep.70237","url":null,"abstract":"<p><strong>Background: </strong>To investigate whether miR-145-5p regulates high-glucose-induced ferroptosis and injury in renal tubular epithelial cells through the KLF4/SIRT3/GPX4 signaling axis. Ferroptosis, a regulated form of iron-dependent cell death, has been increasingly implicated in DKD pathogenesis. The present investigation was designed to explore the functional significance and underlying molecular mechanisms of the miR-145-5p/KLF4/SIRT3/GPX4 signalling cascade in ferroptotic cell death of renal tubular epithelial cells during DKD.</p><p><strong>Methods: </strong>A high-glucose-stimulated in vitro DKD model was constructed using human renal tubular epithelial cells (HK-2) exposed to 25.0 mmol/L glucose. Gene and protein expression profiles were characterised through RT-qPCR, Western blotting and immunofluorescence staining. Cellular viability, apoptotic rates and ferroptosis-associated biomarkers were quantified using CCK-8 assay, flow cytometric analysis, ELISA and JC-1 mitochondrial probe, respectively. Molecular binding interactions were confirmed through dual luciferase reporter assays and co-immunoprecipitation experiments. Intracellular reduced glutathione (GSH) content and GPX4 enzymatic activity were additionally measured to evaluate the functional status of the antioxidant arm of ferroptosis.</p><p><strong>Results: </strong>High glucose exposure triggered time-dependent cellular damage and ferroptotic responses in HK-2 cells, characterised by elevated miR-145-5p levels alongside diminished KLF4, SIRT3 and GPX4 expression. Forced expression of miR-145-5p aggravated cellular damage and ferroptotic phenotypes, whilst its functional suppression conferred cytoprotection. Mechanistic analyses demonstrated that miR-145-5p directly engages the 3'-UTR of KLF4 to repress its expression. Restoring KLF4 expression attenuated high-glucose-mediated cellular injury and enhanced SIRT3 and GPX4 levels. Co-immunoprecipitation assays verified a physical protein-protein association between KLF4 and SIRT3. Functionally, HG stimulation reduced intracellular GSH content and GPX4 enzymatic activity. These changes were aggravated by miR-145-5p overexpression but were partially reversed by miR-145-5p inhibition or KLF4 overexpression.</p><p><strong>Conclusion: </strong>In the context of hyperglycemia, miR-145-5p facilitates ferroptotic cell death in renal tubular epithelial cells through KLF4 suppression, consequently attenuating the SIRT3/GPX4 signalling cascade and worsening DKD-related cellular injury. This regulatory axis may constitute a promising molecular intervention target for DKD treatment.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 8","pages":"e70237"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148582056","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":"Optimising Therapeutic Target Attainment in Vancomycin Therapy for Patients Requiring Intermittent Haemodialysis.","authors":"Danny Tsai, María Patricia Hernández-Mitre, Amy Legg, Jacqueline Martin, Cherian Sajiv, Sachin Kodgire, William Naughton, Sonja Janson, Jaquelyne T Hughes, Xin Liu, Jason A Roberts","doi":"10.1111/nep.70239","DOIUrl":"10.1111/nep.70239","url":null,"abstract":"<p><strong>Aims: </strong>To describe the pharmacokinetics of vancomycin in patients requiring intermittent haemodialysis (iHD) and provide guidance for optimised dosing for a three-times-weekly post-iHD regimen.</p><p><strong>Methods: </strong>A population pharmacokinetic study using retrospectively collected data was conducted in a remote Australian dialysis centre. Adult patients receiving post-iHD vancomycin therapy between 1st January 2017 and 31st July 2023 were screened.</p><p><strong>Inclusion criteria: </strong>≥ 3 months of iHD, prescribed vancomycin, and recorded ≥ 1 vancomycin concentration. Pharmacokinetic analysis was performed using Monolix. The probability of pharmacokinetic/pharmacodynamic target attainment (PTA) for pre-iHD trough concentrations of 15-20 mg/L was simulated for various loading and maintenance doses.</p><p><strong>Results: </strong>A total of 302 vancomycin concentrations were available from 80 courses (58 patients, 45 were female) with a median age of 52 (IQR 45-61) years and weight of 75 (66.5-85.5) kg. A one-compartment model adequately described the data. Actual body weight was the only covariate retained in the final model. The estimated vancomycin clearance during non-iHD periods, during iHD periods, and volume of distribution were 0.54 L/h, 4.84 L/h, and 87.02 L, respectively. The simulations supported weight-based loading doses. The time to the next iHD session also significantly influenced the PTA of loading doses. Subjects with higher weight required lower weight-based doses, and vice versa. The PTA of maintenance doses was associated with the pre-iHD trough concentrations and the dosing intervals. Weight had a limited impact on the PTA of maintenance doses.</p><p><strong>Conclusion: </strong>A comprehensive vancomycin dosing nomogram was suggested for patients requiring iHD. Validation in future prospective studies is recommended.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70239"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348660","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":"Serum Response Factor Regulates CCN1 to Exacerbate Acute Kidney Injury Through Facilitation of Ferroptosis-Related Injury.","authors":"Yanfei Wang, Chen Guan, Chenyu Li, Wei Jiang, Hong Luan, Congjuan Luo, Quandong Bu, Haiyan Zhou, Wei Zhang, Liting Wang, Yue Zhang, Ningxin Zhang, Yan Xu, Long Zhao","doi":"10.1111/nep.70244","DOIUrl":"10.1111/nep.70244","url":null,"abstract":"<p><strong>Aim: </strong>To explore the regulation and function of serum response factor (SRF)/Cellular communication network factor 1 (CCN1) pathway in ferroptosis in ischemia/reperfusion (I/R) acute kidney injury (AKI).</p><p><strong>Methods: </strong>The level of SRF, CCN1, ferroptosis markers (TFR1, ACSL4, xCT, GPX4), ROS and SOD were examined in HK-2 cells under hypoxia/reoxygenation (H/R) treatment or rat renal tissue samples after I/R treatment. SRF was overexpressed by pcDNA-SRF plasmid and suppressed by CCG-1423 (a small molecule inhibitor of SRF) or SRF siRNA to study how SRF influences ferroptosis through CCN1 in I/R AKI.</p><p><strong>Results: </strong>In HK-2 cells under H/R treatment and renal tissue from I/R rats, the SRF along with CCN1, TFR1 and ACSL4 expression was upregulated, while xCT and GPX4 expression was downregulated. SRF upregulation in HK-2 cells increased CCN1 expression and was associated with ferroptosis-related changes. Blockade of SRF by CCG-1423 or an SRF-specific siRNA reduced CCN1 induction, protected renal tubular epithelial cells from ferroptosis-related injury, and alleviated I/R AKI both in vitro and in vivo.</p><p><strong>Conclusion: </strong>Increased SRF/CCN1 pathway activity may be associated with ferroptosis-related injury and dysfunction in renal tubular epithelial cells during AKI. Targeting SRF with CCG-1423 may represent a potential therapeutic strategy of AKI.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70244"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148407823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Injury to E- and VE-Cadherin in Paediatric Idiopathic Steroid-Sensitive Nephrotic Syndrome: Potential Markers of the Disease Status.","authors":"Takahiro Kanai, Jun Aoyagi, Masanori Kurosaki, Tomomi Maru, Marika Ishii, Toshihiro Tajima","doi":"10.1111/nep.70240","DOIUrl":"https://doi.org/10.1111/nep.70240","url":null,"abstract":"<p><strong>Aim: </strong>The pathophysiology of idiopathic steroid-sensitive nephrotic syndrome (ISSNS) remains unclear. This study aimed to explore the pathophysiology by examining E-cadherin injury, observed in atopic dermatitis, and VE-cadherin injury, associated with systemic edema formation.</p><p><strong>Methods: </strong>Twenty-one paediatric patients with ISSNS were enrolled. Serum E- and VE-cadherin levels were measured using ELISA and compared between the nephrotic and remission phases. Correlations between each serum E- and VE-cadherin level and urinary protein/creatinine (UP/UCr) ratios and serum albumin (Alb) levels were analysed. Additionally, a correlation between changes in serum VE-cadherin levels and in body weight between phases was analysed.</p><p><strong>Results: </strong>Both serum E- and VE-cadherin levels were elevated in the nephrotic phase compared to the remission phase (p < 0.01 for both). Remission-phase E-cadherin levels remained higher than those in healthy children, while remission-phase VE-cadherin levels were similar to those in healthy children. Serum E-cadherin levels showed a significant correlation with UP/UCr ratios (p = 0.04), but not with serum Alb levels. Serum VE-cadherin levels did not correlate with either UP/UCr ratios or serum Alb levels. However, changes in VE-cadherin levels between the phases were significantly correlated with changes in body weight (p = 0.04).</p><p><strong>Conclusion: </strong>Elevated E- and VE-cadherin levels during the nephrotic phase suggest that injury to these adhesion molecules may be correlated with the disease status and could serve as biomarkers for paediatric ISSNS. Injury to E-cadherin may contribute to proteinuria while injury to VE-cadherin may lead to systemic edema. These findings provide new insights into paediatric ISSNS pathophysiology.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70240"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CORO1A, A Novel Upregulated Protein in Renal Tubular Epithelial Cells of Diabetic Nephropathy, Participates in Regulating Vesicular Trafficking and the Ferroptosis Pathway.","authors":"Shenghao Meng, Xitong Xu, Hongru Chen, Zhigang Zhang, Huijuan Wu, Chenyang Qi","doi":"10.1111/nep.70246","DOIUrl":"10.1111/nep.70246","url":null,"abstract":"<p><strong>Aim: </strong>Diabetic nephropathy (DN) is characterised by progressive renal tubular epithelial cell injury, yet underlying molecular mechanisms remain incompletely understood.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) in DN were identified through integrated GEO dataset analysis (GSE30529 and GSE175759). Protein-protein interaction networks identified hub genes. GO and KEGG enrichment analyses determined molecular mechanisms. Nephroseq v5 explored correlations between hub genes and clinical features. CORO1A expression was validated by immunohistochemistry and western blot in DN patients, diabetic db/db mice and high glucose-exposed HK-2 cells. Vps34 inhibition and CORO1A knockdown explored regulatory mechanisms in vesicular trafficking and ferroptosis.</p><p><strong>Results: </strong>Bioinformatics identified CORO1A as a phagosome-related core gene significantly upregulated in DN renal tubulointerstitium and correlated with eGFR, proteinuria, serum creatinine, blood pressure and age. External validation and experiments confirmed CORO1A upregulation in DN patients, diabetic mice and high glucose-exposed cells. Vps34 inhibition impaired lysosomal degradation flux and increased tubular injury markers, ferroptosis, ferritinophagy and CORO1A expression. CORO1A knockdown attenuated ferroptosis and lipid peroxidation, while rescue experiments with Ferrostatin-1 and Erastin confirmed the functional link between CORO1A, vesicular trafficking and ferroptosis.</p><p><strong>Conclusion: </strong>CORO1A is elevated in diabetic renal tubular epithelial cells and regulates vesicular trafficking and ferroptosis. This mechanistic axis suggests CORO1A as a potential therapeutic target for mitigating tubular injury and diabetic nephropathy progression.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70246"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13376232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148475736","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":"Efficacy of Reticulocyte Haemoglobin Equivalent-Guided Versus Transferrin Saturation-Guided Iron Supplement Protocol in Haemodialysis Patients: A Multicenter Cluster Randomized Controlled Trial.","authors":"Chalermchon Suttaluang, Jeerath Phannajit, Monchai Siribamrungwong, Kamonrat Chongthanakorn, Songkiat Lewsuwan, Pisut Katavetin, Yingyos Avihingsanon, Kearkiat Praditpornsilpa, Somchai Eiam-Ong, Kullaya Takkavatakarn, Paweena Susantitaphong","doi":"10.1111/nep.70247","DOIUrl":"10.1111/nep.70247","url":null,"abstract":"<p><strong>Background: </strong>Iron deficiency is common in patients receiving haemodialysis and contributes to adverse outcomes. Conventional iron biomarkers, including ferritin and transferrin saturation (TSAT), have limitations and may be less accessible in some settings. Reticulocyte haemoglobin equivalent (RET-He) is a lower-cost, potentially more accessible marker for detection of iron deficiency. This study evaluated whether RET-He-guided intravenous iron supplementation is non-inferior to TSAT-guided supplementation in haemodialysis patients.</p><p><strong>Methods: </strong>In this randomized non-inferiority trial, 160 haemodialysis patients were randomized to a TSAT-guided group (n = 79) or RET-He-guided group (n = 81). Intravenous iron was administered in both groups according to prespecified protocols. The primary outcome was the erythropoietin resistance index (ERI) at 3 and 6 months. RET-He guidance was considered non-inferior if the upper bound of the 95% confidence interval (CI) for the between-group mean difference was ≤ 160 units/week/g/dL. Secondary outcomes included all-cause mortality, hospitalization, cardiovascular events, blood transfusion, and infection.</p><p><strong>Results: </strong>Baseline characteristics were comparable between groups. RET-He-guided supplementation was non-inferior to TSAT-guided supplementation for ERI at 3 months (mean difference, -35.92; 95% CI, -155.60 to 90.29; p = 0.001 for non-inferiority) and 6 months (mean difference, -39.68; 95% CI, -187.01 to 107.64; p = 0.004 for non-inferiority). The RET-He group received significantly lower cumulative intravenous iron doses. Secondary outcomes did not differ significantly, although the trial was not powered for these clinical outcomes.</p><p><strong>Conclusion: </strong>RET-He-guided intravenous iron supplementation was non-inferior to TSAT-guided supplementation for reducing ERI over 6 months. Use of RET-He may offer a lower-cost and more accessible strategy for anaemia management in haemodialysis patients, particularly in resource-limited settings.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70247"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13385484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148537671","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}