American Journal of Nephrology最新文献

{"title":"Additive Obinutuzumab in Rituximab-refractory Membraneous Nephropathy: Caution in Effect Attribution.","authors":"Emre Cankaya, Burak Aslum, Ezgi Çoskun Yenigun","doi":"10.1159/ajn/ablag009","DOIUrl":"https://doi.org/10.1159/ajn/ablag009","url":null,"abstract":"","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monitoring Long-term Tacrolimus Exposure: Metrics, Trajectories, and Associations with Outcomes after Kidney Transplantation in the Wisconsin Allograft Recipient Database (WisARD).","authors":"Zhongyu Yuan, Sandesh Parajuli, Didier Mandelbrot, Brad C Astor","doi":"10.1159/000552040","DOIUrl":"https://doi.org/10.1159/000552040","url":null,"abstract":"<p><p>Background There is no consensus on the optimal metric for long-term tacrolimus monitoring after kidney transplantation. It remains unknown how tacrolimus exposure changes over time and how tacrolimus monitoring metrics are related to long-term outcomes. Methods We examined tacrolimus exposure beyond the first year after kidney transplantation, as assessed by multiple monitoring metrics (i.e., mean trough level, intra-patient variability [IPV], time in therapeutic range [TTR], time below range, time above range), in the Wisconsin Allograft Recipient Database. We examined associations of these metrics with late graft outcomes (late rejection, uncensored and death-censored graft failure [DCGF]) and mortality (death with a functioning graft [DWFG]). Results A total of 1994 kidney transplant recipients, who received tacrolimus-based immunosuppression and survived at least 12 months with a functioning graft, were included. We observed a decreasing trend of tacrolimus exposure over median follow-up of 5.3 years. A high tacrolimus IPV (coefficient of variation ≥30%) in the second year was most strongly associated with outcomes, including a 45% higher risk of uncensored graft failure (adjusted hazard ratio =1.45; 95% confidence interval: 1.22, 1.72; p <0.01). A higher IPV also was associated with a higher risk of death-censored graft failure, mortality, and late rejection. Cumulative high tacrolimus IPV in the past 5 years was associated with higher risk of graft failure and mortality. Conclusion Metrics of tacrolimus exposure assessed beyond the first year after kidney transplantation, especially IPV, remain informative for long-term outcomes.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-23"},"PeriodicalIF":3.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Barriers to Person-Centered CKD Care: A Qualitative Study of Multidisciplinary Nephrology Clinicians.","authors":"In-Gu Kang, JoAnn S Oliver, Nayoung Kim, Ashley Abawi, Audrey Boahemaa Kusi, Felecia G Wood, Pamela P Foster, Sharlene D Newman","doi":"10.1159/ajn/ablag007","DOIUrl":"https://doi.org/10.1159/ajn/ablag007","url":null,"abstract":"<p><strong>Introduction: </strong>The clinician-identified barriers to person-centered chronic kidney disease (CKD) care remain poorly characterized among socioeconomically disadvantaged populations. We examined nephrology clinicians' perspectives on patient preparation, dialysis decision-making, and structural barriers to inform multilevel intervention.</p><p><strong>Methods: </strong>A qualitative descriptive study using semi-structured interviews and thematic analysis following Braun and Clarke's (2006) approach [29] included 22 English-speaking nephrology clinicians recruited via snowball sampling. Transcripts were analyzed thematically.</p><p><strong>Results: </strong>Three themes emerged. First, CKD awareness, education, and preparedness: patient awareness was uneven and often absent even under nephrology care; education was multidisciplinary and stage-sensitive but emotionally constrained. Second, dialysis decision-making: planned outpatient initiation was distinguished from unplanned emergency starts, the latter associated with reduced patient choice and worse outcomes; modality discussions typically began at an estimated glomerular filtration rate (eGFR) of approximately 20 mL/min/1.73m² but timing varied widely; nephrology clinicians sometimes omitted home dialysis options when patient support seemed uncertain; and family involvement was central to adherence and decision quality. Third, barriers, supports, and clinical management: nonadherence reflected structural barriers, financial hardship, health literacy, transportation, and delayed referral, rather than motivation, while the clinician-patient relationship was a modifiable adherence determinant limited by understaffed support services.</p><p><strong>Discussion: </strong>Nephrology clinicians identified patient awareness, education timing, provider variability, and structural barriers as modifiable determinants of inequitable CKD outcomes. Multilevel intervention targeting pre-dialysis education, primary care coordination, reimbursement reform, and social support infrastructure is needed.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adynamic Bone Disease in Chronic Kidney Disease: From PTH Suppression-Driven Remodeling Phenotype to Osteoanabolic Therapy.","authors":"Kuo-Cheng Lu, Yi-Chou Hou, Chia-Chao Wu, Te-Chao Fang, Kuo-Chin Hung, Chien-Lin Lu","doi":"10.1159/ajn/ablag003","DOIUrl":"https://doi.org/10.1159/ajn/ablag003","url":null,"abstract":"<p><strong>Background: </strong>Adynamic bone disease (ABD) is an increasingly prevalent form of low-turnover renal osteodystrophy in advanced chronic kidney disease (CKD). ABD was not recognized as a clinical entity prior to the widespread adoption of PTH-targeted therapeutic strategies, and sustained iatrogenic suppression of parathyroid hormone (PTH) activity is now understood as the primary and defining causal mechanism underlying the adynamic phenotype. Uremic toxins, FGF-23-Klotho dysregulation, impaired vitamin D signaling, chronic inflammation, calcium-phosphate imbalance, and osteocyte-mediated abnormalities function as modulatory contributors that amplify skeletal susceptibility within the context of sustained PTH suppression, rather than independent drivers of ABD. Clinically, ABD is associated with impaired bone quality, increased fracture risk, vascular calcification, and musculoskeletal frailty, abnormalities that are often not adequately reflected by areal bone mineral density measurements alone.</p><p><strong>Summary: </strong>ABD in advanced CKD represents a PTH suppression-driven skeletal remodeling phenotype characterized by osteoblast, osteoclast, and osteocyte dysfunction together with disruption of osteoblast-osteoclast coupling. Suppression of Wnt/β-catenin signaling, elevated sclerostin expression, impaired mechanotransduction, skeletal resistance to PTH, and accumulation of uremic toxins collectively contribute to globally reduced remodeling activity and defective microdamage repair. In the context of markedly suppressed bone turnover, antiresorptive therapy is biologically unlikely to confer skeletal benefit and may exacerbate impairment of bone remodeling and renewal. By contrast, anabolic strategies aimed at restoring PTH1R-dependent bone formation and remodeling activation are mechanistically appropriate in CKD-associated ABD. Current evidence suggests that intermittent PTH analog therapy, particularly teriparatide, may improve bone formation markers, bone mineral density, and remodeling activity in selected CKD patients with low-turnover bone disease. Abaloparatide is mechanistically promising but clinically unvalidated in advanced CKD. Romosozumab should not be used in clinical practice for CKD-associated ABD given profound uncertainties regarding cardiovascular safety, vascular calcification, and calcium handling in this population. Practical considerations regarding patient selection, biochemical monitoring, prevention of ABD through avoidance of prolonged PTH suppression, and individualized treatment strategies are also discussed.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148862999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Factors Associated with Hyperkalemia in Chronic Kidney Disease: Insights from a Cohort with Measured Glomerular Filtration Rate.","authors":"Justina Motiejunaite, Martin Flamant, Alexandre Lahens, Timothée Fearon, Nahid Tabibzadeh, Anne Boutten, François Vrtovsnik, Bénédicte Stengel, Natalia Alencar de Pinho, Emmanuelle Vidal-Petiot","doi":"10.1159/ajn/ablag008","DOIUrl":"https://doi.org/10.1159/ajn/ablag008","url":null,"abstract":"<p><strong>Introduction: </strong>Hyperkalemia is a life-threatening disorder in chronic kidney disease (CKD), yet the contribution of key factors including age, sex, body mass index and proteinuria remain controversial. We aimed to identify factors associated with chronic hyperkalemia in a large cohort of patients with gold-standard measured glomerular filtration rate (GFR) and standardized plasma potassium measurements.</p><p><strong>Methods: </strong>This cross-sectional study of 5046 adults with non-dialysis CKD referred for kidney workup, including radio-isotopic measured GFR, defined hyperkalemia as a plasma potassium concentration ≥5.0 mmol/L or the use of potassium binders. We analyzed demographic, clinical, pharmacological and biochemical risk factors for hyperkalemia using logistic regression models.</p><p><strong>Results: </strong>Mean measured GFR was 59±26 mL/min/1.73 m2, mean age was 52±15 years, 42% were women, 22% of sub-Saharan African ancestry, 25% had diabetes, and 36% were kidney transplant recipients. The prevalence of hyperkalemia was 6.4% and increased with declining measured GFR, from 1% in CKD stages 1-2 to 8% in CKD stage 3 and 21% in stages 4-5. In the multivariable model, measured GFR remained strongly associated with hyperkalemia (OR 1.65 [1.51-1.81] per 10 mL/min/1.73m² decrease), an effect amplified in renin-angiotensin-aldosterone system inhibitor (RAASi) users (1.82 [1.61-2.07]) (p for interaction 0.036). Other independently associated factors were diabetes (OR 1.67 [1.38-2.17]), RAASi and calcineurin inhibitors (OR 2.30 [1.72-3.11] and 1.39 [1.06-1.83] respectively), higher urinary albumin-to-creatinine ratio and lower venous bicarbonate level, whereas female sex (OR 0.71 [0.55-0.92]), sub-Saharan African ancestry (HR 0.68 [0.48-0.94]), and loop-diuretics (OR 0.71 [0.51-0.98]) were protective, and age and body mass index showed no independent association.</p><p><strong>Conclusion: </strong>In this large cohort, across the entire range of gold-standard measured GFR, hyperkalemia is driven primarily by reduced kidney function, diabetes, and RAASi, whereas protective factors were female sex, sub-Saharan African ancestry, and loop diuretic therapy. These robust findings, based on unbiased GFR assessment, identify key contributors for individualized prevention of hyperkalemia in CKD.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risks of Major Adverse Kidney Events in Non-Hispanic Black Patients with Diabetes or Hypertension: A real-world cohort study.","authors":"Kiara N Mayhand, Anna Zemke, Radica Alicic, Lindsey M Kornowske, Cami R Jones, Kenneth B Daratha, Christina L Reynolds, Susanne B Nicholas, Roland J Thorpe, Panayiotis Petousis, Leonid Shpaner, Joshua Jon Neumiller, Keith Norris, Katherine R Tuttle","doi":"10.1159/ajn/ablag006","DOIUrl":"https://doi.org/10.1159/ajn/ablag006","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic kidney disease (CKD) disproportionately burdens non-Hispanic Black (NHB) patients who experience a three- to four-fold higher risk of kidney failure than non-Hispanic White (NHW) individuals. Diabetes and hypertension are the leading causes of CKD, yet the influence of race, social context, and clinical factors on major adverse kidney events (MAKE) remains inadequately understood. This study examined relationships between race, social factors, and MAKE among patients with diabetes or hypertension.</p><p><strong>Methods: </strong>Electronic health record data from the CURE-CKD Registry (2013-2022) were used to assemble two mutually-exclusive cohorts of NHB and NHW (reference) adults with 1. diabetes (N=375,605) or 2. Hypertension without diabetes (N=710,768). The primary outcome was time to first MAKE, defined as ≥40% decline in estimated glomerular filtration rate (eGFR), eGFR <15 mL/min/1.73 m², kidney failure, dialysis, transplant, or death. Cox proportional hazards models estimated associations between predictors and MAKE. Extreme gradient boosting (XGBoost) machine learning (ML) models were used as a complement to the traditional survival models to evaluate variable relationships with MAKE and compare predictive performance.</p><p><strong>Results: </strong>NHB patients were younger (diabetes: 56±15 vs. 62±14 years; hypertension: 50±16 vs. 59±16 years), had more prevalent CKD (diabetes: 19% vs. 15%; hypertension: 8% vs. 7%), and had higher adjusted MAKE risk than NHW patients (diabetes: HR=1.07, 95% CI: 1.04-1.11; hypertension: HR=1.10, 95% CI: 1.06-1.14). MAKE occurred in 24% (n=90,910) of the diabetes population over a median (interquartile range) of 4.1 (2.0-6.3) years, and 15% (n=106,209) of the hypertension population over 4.4 (2.4-6.3) years. Non-commercial insurance (Medicaid, Medicare or unclassified insurance [reference: Commercial]), higher social vulnerability index, more frequent hospitalizations, and urban residence were the top predictors of MAKE. XGBoost outperformed Cox models for MAKE prediction and SHapley Additive exPlanations value rankings confirmed key predictors identified in Cox models.</p><p><strong>Conclusion: </strong>Across two large cohorts at-risk for CKD, NHB patients experienced higher MAKE risk, shaped by neighborhood social and structural conditions rather than demographic and clinical characteristics alone. Integrating social risk assessment, improving guideline-directed testing, and using complementary ML and Cox modeling approaches may enhance early identification of CKD risk, support targeted intervention, and reduce disparities in CKD outcomes.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperglycemia and alteration in sphingolipids are early mediators of diabetic kidney disease: role of elongase 1 (Elovl1).","authors":"Waleed O Twal, Peggi M Angel, Kristi L Helke, Alexander Awgulewitsch, Jason Pierce, Rebecca Gregory, Juan Torres, Yuan Shao, Carsten Krieg, Silvia Guglietta, Mrinmoyee Majumder, Nahla Hamouda, Whitney Christians, Harrison B Taylor, Benjamin Caiello, Jake Griner, Samar M Hammad","doi":"10.1159/000552867","DOIUrl":"https://doi.org/10.1159/000552867","url":null,"abstract":"<p><p>Introduction Diabetic kidney disease (DKD) is characterized by impairment of renal glomerular and tubular cells. Low plasma levels of ceramides and lactosylceramides containing very long-chain (VLC) fatty acid were found to be predictive of DKD development. Elongase 1 (Elovl1) is a ubiquitous elongase that elongates C20-C22 fatty acids to generate very long-chain C24 fatty acids. Using a novel transgenic mouse overexpressing Elovl1, we investigated whether modification to sphingolipid fatty acid composition averts DKD development. Methods A transgenic (TG) mouse overexpressing Elovl1 was created at the Medical University of South Carolina/Transgenic Core. Elovl1 TG and wild type (WT) mice were rendered diabetic using serial streptozotocin injections. Plasma, kidney, liver, and urine sphingolipidomics of diabetic and non-diabetic TG and WT mice were analyzed using mass spectroscopy and Matrix-Assisted Laser Desorption/Ionization-Imaging Mass Spectrometry. Sphingolipid metabolizing enzymes were analyzed using immunohistochemical & multispectral imaging coupled with digital analysis. Results Plasma sphingomyelins were higher, but lactosylceramides were lower in diabetic TG than in diabetic WT mice. Kidney lactosylceramides were also lower in diabetic TG mice. In urine, diabetic TG mice excreted more VLC lactosylceramides than diabetic WT mice, but less VLC sphingomyelins, VLC ceramides, sphingosine and sphingosine 1-phosphate. There was extensive damage to proximal tubules in kidneys of diabetic WT mice compared to diabetic TG mice. Glomeruli in diabetic WT kidneys appeared also abnormal, whereas no obvious abnormality of glomeruli in diabetic TG was observed. In diabetic TG, Elovl1 overexpression resulted in decreased kidneys levels of both ceramide synthase and acid sphingomyelinase, but increased acid ceramidase levels compared to non-diabetic TG mice. Conclusion The diabetic Elovl1 TG mouse revealed interaction between Elovl1 overexpression and DKD development, and showed that distinct VLC sphingolipids could be involved in maintaining cell membrane integrity of renal cells.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-30"},"PeriodicalIF":3.8,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Regulation of CCN1 Contributes to Skeletal Muscle Wasting in Chronic Kidney Disease.","authors":"Yidan Zuo, Ruyi Chen, Diyan Xu, Wenli Zhang, Shengnan Luo, Feifei Hu, Zhen Su","doi":"10.1159/000553578","DOIUrl":"https://doi.org/10.1159/000553578","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is a prevalent complication of chronic kidney disease (CKD), yet reliable biomarkers remain limited. CCN1, a matricellular protein involved in cellular senescence, has been implicated in muscle wasting, but its role in CKD-associated muscle strength decline is incompletely understood.</p><p><strong>Methods: </strong>Serum CCN1 levels were measured by ELISA in 40 stage 3-5 CKD patients and 27 age-matched controls and correlated with handgrip strength (HGS). A 5/6 nephrectomy (NX) mouse model was established to evaluate muscle strength and senescence markers. C2C12 myotubes were treated with recombinant CCN1 or Wnt3a, with or without integrin β1 inhibitor or DKK-1. Senescence-associated β-galactosidase staining, qPCR, Western blot, co immunoprecipitation, and immunofluorescence were performed to explore mechanisms.</p><p><strong>Results: </strong>GEO database analysis and our clinical data showed significantly elevated serum CCN1 levels in CKD patients versus controls. A trend toward a negative association was observed between serum CCN1 levels and HGS. In NX mice, reduced grip strength was associated with increased skeletal muscle CCN1 expression, upregulation of p53/p21/p16, and elevated Fbx32/Trim63. Co immunoprecipitation revealed physical interaction between CCN1 and integrin α6/β1. Blockade of integrin β1 attenuated CCN1 induced myotube senescence. Wnt3a dose dependently upregulated CCN1 and senescence markers, while DKK-1 partially reversed these effects. Serum from CKD mice with muscle wasting directly induced senescence in C2C12 myotubes, an effect also mitigated by DKK-1.</p><p><strong>Conclusions: </strong>CCN1 promotes muscle senescence through integrin α6/β1 signaling, with Wnt3a as an upstream regulator. CCN1 may serve as a potential biomarker for CKD related muscle wasting, and targeting the Wnt3a CCN1 integrin axis could represent a novel therapeutic strategy.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1-24"},"PeriodicalIF":3.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to letter by dr L. Gao, on 'Lower Risk of Acute Kidney Injury in Hospitalized Patients Treated With SGLT-2 Inhibitors: A Retrospective Matched Cohort Study'.","authors":"Dion Gabriël Lodewijk de Martines, Kenan Hasan Ali Aydinoglu, Christina Maria Gant, Kim de Jong, Aaltje Ymkje Adema","doi":"10.1159/ajn/ablag004","DOIUrl":"https://doi.org/10.1159/ajn/ablag004","url":null,"abstract":"<p><p>We thank Gao and Lu for their thoughtful comments on our study investigating the association between sodium-glucose cotransporter-2 inhibitor (SGLT-2i) use and acute kidney injury (AKI) risk in hospitalised patients. In this reply, we clarify several methodological and interpretative aspects of our study. In particular, secondary analyses of continuation, discontinuation and initiation of SGLT-2i during hospitalisation should be interpreted cautiously, as these treatment decisions are likely influenced by clinical stability and other unmeasured factors. We further address concerns regarding AKI ascertainment, baseline creatinine selection, indication-stratified analyses, and the limited feasibility of dose- or agent-specific comparisons. Additional sensitivity analyses did not suggest major imbalance in early AKI detection between groups. Overall, we agree that the findings of our secondary analysis should be considered hypothesis-generating rather than definitive evidence for inpatient continuation of SGLT-2i. Future studies using prospective designs, time-updated exposure modelling or target trial emulation are needed to determine which patients may safely benefit from continuation during hospitalisation.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Statement.","authors":"","doi":"10.1159/000553196","DOIUrl":"10.1159/000553196","url":null,"abstract":"<p><p>The article \"Tonsillar CD4+CD25+ Regulatory T Cells from IgA Nephropathy Patients Have Decreased Immunosuppressive Activity in Experimental IgA Nephropathy Rats\" [Am J Nephrol. 2013;37(5):472-480; https://doi.org/10.1159/000350533] by Hongdong Huang, Youming Peng, Xi-Dai Long, Zhihua Liu, Xiaojun Wen, Meng Jia, Yumei Liang, and Anlan Huang has been retracted by the Publisher and the Editor.After the publication of this article, image duplication was identified between Figure 3 (TGF-β1) and Figure 3 (β-actin) of this article and Figure 3 (ADAMTSI3-antibody) and Figure 3 (β-actin), respectively, in a later published article by overlapping authors [1]. Image duplication was also detected between the panels within Figure 4 of this article.When asked to comment, the corresponding author stated that the original data for Figure 3 was not available for review and did not provide an explanation for the overlapping images. The authors provided an original image for Figure 4. The concerns and authors' response were reviewed by the Editor, who determined that the response was unsatisfactory to resolve the concerns and concluded that, as the concerns are not resolved and may impact the reliability of the article, the article should be retracted.Hongdong Huang disagrees with the retraction, and the co-authors did not respond to our correspondence about the retraction of this article within the timeframe specified or could not be reached for comment.</p>","PeriodicalId":7570,"journal":{"name":"American Journal of Nephrology","volume":" ","pages":"1"},"PeriodicalIF":3.8,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148719928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}