BackgroundJehovah’s Witnesses (JWs) refuse blood transfusions on religious grounds, creating a major challenge in kidney transplantation (KT), where perioperative bleeding may necessitate transfusion support. Evidence regarding transfusion-free KT in JWs remains limited. We evaluated the feasibility and early clinical outcomes of a transfusion-free KT protocol in JW patients.MethodsWe performed a single-centre propensity score–matched cohort study including all JW recipients who underwent KT under a transfusion-free protocol between 2016 and 2025. The protocol included pre-transplant haemoglobin optimisation to ≥13 g/dL. JW recipients were matched 1:3 to non-JW controls based on recipient age and sex, donor type, and transplant date. Outcomes included peri-transplant transfusion, anaemia management, bleeding-related complications, and early post-transplant results.Results27 JW recipients and 74 controls were included. Peri-transplant transfusion was completely avoided in JW recipients (0/27), whereas 24/74 controls (32.4%) required transfusion support. Bleeding-related complications occurred in 14.8% of JW recipients and 11.3% of controls (RR 1.65, 95% CI 0.44–6.21). Admission haemoglobin was higher in JW recipients (14.2 vs 11.5 g/dL; MD 2.69, 95% CI 2.15–3.22), as was nadir haemoglobin (10.0 vs 8.5 g/dL; MD 1.50, 95% CI 0.55–2.45). However, the absolute decrease from admission to nadir was greater in JW recipients (4.14 vs 3.01 g/dL; MD 1.13, 95% CI 0.21–2.06). Hospital stay was longer in JW recipients (MD 5.2 days, 95% CI −0.10 to 10.31).ConclusionsA transfusion-free KT protocol was feasible in JW recipients managed at an experienced centre and enabled complete avoidance of peri-transplant transfusion. Early outcomes are reported descriptively and should be interpreted with caution because of the small sample size and residual imbalance between groups.
BackgroundAnemia is highly prevalent in patients with kidney failure receiving peritoneal dialysis (PD). Oral iron supplementation is frequently prescribed, but adherence may be limited by pill burden and gastrointestinal adverse effects. Emerging evidence suggests that less frequent oral iron dosing may enhance iron absorption by reducing hepcidin-mediated inhibition, yet data in PD patients are lacking. We evaluated iron utilization and compared the effectiveness of different oral iron regimens in PD patients.MethodsThis retrospective cohort study (2007-2025) included adults (≥18 years) receiving peritoneal dialysis at the Dialysis Center Groningen who were treated with oral ferrous fumarate for ≥3 months. Patients receiving intravenous iron, other iron formulations, non-standard dosing regimens, or with active gastrointestinal bleeding were excluded. Ferrous fumarate regimens included 200 mg once daily (OD), twice daily (BID), three times daily (TID), or three times weekly (TIW). Patients not receiving oral iron were evaluated for treatment eligibility. Primary outcomes were 6-month changes in hemoglobin, ferritin, and transferrin saturation. Regimen-specific trajectories were analyzed using linear mixed-effects models. Sensitivity analyses adjusted for age, sex, erythropoiesis-stimulating agent dose, and inflammation, and were restricted to incident iron users on PD.ResultsOf the 140 patients screened, 85 patients were included (median age 61 years; 57.6% male). TIW dosing resulted in hemoglobin trajectories comparable to OD dosing (P = 0.30), with similar ferritin and transferrin saturation trajectories. In contrast, BID dosing was associated with a steeper hemoglobin increase (0.013 g/dL/day; P = 0.001) than OD dosing. Sensitivity analyses yielded similar results. Among patients not receiving iron therapy, 30% (n= 9/30) met contemporaneous guideline criteria for treatment.ConclusionIn this 18-year retrospective study of 85 PD patients, TIW and OD oral iron supplementation produced comparable hematologic outcomes, suggesting that less frequent dosing may represent an effective strategy to reduce treatment burden without compromising efficacy. Twice-daily dosing was associated with faster hemoglobin increases, likely reflecting greater cumulative iron exposure. Iron therapy was underutilized in a substantial proportion of eligible patients. Although limited by the modest sample size, these findings highlight the need for expert consensus to address evidence gaps and guide anemia management in PD.
BackgroundAcute kidney injury (AKI) occurs across a heterogeneous population with substantial variation in comorbidity burden. Although multimorbidity is associated with adverse outcomes in AKI, whether mortality increases progressively with disease burden or varies according to the extent and composition of coexisting conditions remains unclear. We examined the association between selected comorbidity burden and in-hospital mortality among U.S. adults hospitalized with AKI.MethodsWe conducted a retrospective cross-sectional study using the 2022 National Inpatient Sample. Adult hospitalizations with AKI were identified using ICD-10-CM codes. Comorbidity burden was defined as the number of six conditions—diabetes, hypertension, heart failure, non-ESRD chronic kidney disease, liver disease, and malignancy—and evaluated as counts from 0 to 6. Survey-weighted logistic regression estimated associations with in-hospital mortality after adjustment for demographic, admission, and hospital characteristics. Functional form was evaluated using linear, spline, and categorical specifications. Population-standardized mortality probabilities were estimated, with additional analyses examining acute illness, disease composition, and hospital location/teaching status.ResultsThe cohort included 1,066,687 hospitalizations, representing 5.33 million U.S. hospitalizations with AKI. The association between comorbidity burden and mortality was nonlinear. Relative to count 0, adjusted mortality odds were lower at counts of two (aOR, 0.83; 95% CI, 0.80–0.86), three (aOR, 0.77; 95% CI, 0.74–0.80), and four (aOR, 0.79; 95% CI, 0.76–0.82), but higher at counts of five (aOR, 1.27; 95% CI, 1.20–1.34) and six (aOR, 1.52; 95% CI, 1.27–1.82). Population-standardized mortality was 9.92% at count 0, 7.83% at count 3, 12.20% at count 5, and 14.25% at count 6. Adjustment for sepsis and mechanical ventilation attenuated differences at intermediate levels, whereas elevated mortality at counts five and six persisted across models. Disease composition influenced the high-burden association; elevated mortality at count five persisted after exclusion of malignancy but not liver disease. Hospital location/teaching status interacted with burden (P for interaction=0.028), although absolute mortality differences were modest.ConclusionsAmong U.S. adults hospitalized with AKI, selected comorbidity burden was nonlinearly associated with in-hospital mortality. The relationship reflected the number and composition of coexisting conditions and acute illness context, cautioning against interpreting comorbidity count as a uniform linear risk gradient or fixed clinical threshold.
Background and objectivesArtificial intelligence (AI) is increasingly being applied across nephrology, with potential applications spanning disease prediction, diagnosis, treatment optimisation, and clinical decision support. However, reported model performance varies substantially across clinical domains, and high predictive performance does not necessarily demonstrate clinical utility or readiness for deployment. This narrative review synthesizes current evidence on the applications of AI in nephrology and critically evaluates the methodological maturity, validation, interpretability, fairness, and translational readiness of AI systems across major nephrology domains.MethodsA structured literature search of PubMed was conducted using terms related to AI and nephrology, with the primary eligibility period restricted to studies published from 2020 to 2025. The search strategy incorporated artificial intelligence, machine learning, deep learning, neural networks, natural language processing, large language models, generative AI, computer vision, reinforcement learning, federated learning, and related terms, together with nephrology and kidney-disease terms. Title/abstract and full-text screening were performed independently by the first and second authors, with disagreements resolved by the third author. Two foundational pre-2020 studies identified through citation chaining were retained because of their importance to the subsequent development of AI applications in nephrology. Evidence was synthesized qualitatively according to study design, validation, predictive performance, interpretability, fairness, prospective evaluation, and translational readiness.ResultsAI applications were identified across acute kidney injury, chronic kidney disease, nephropathology, kidney transplantation, haemodialysis, peritoneal dialysis, large language models, reinforcement learning, and federated learning. Across these domains, many models demonstrated promising discrimination, but evidence maturity varied considerably. External validation was present for some applications, whereas prospective evaluation and evidence of clinical utility remained limited. The literature also highlighted challenges related to calibration, generalizability, interpretability, algorithmic fairness, data governance, and integration into clinical workflows. Large language models and federated learning represent emerging areas, but nephrology-specific evidence remains comparatively limited.ConclusionsAI has substantial potential to support precision nephrology, but technical performance should not be equated with clinical effectiveness or deployment readiness. Future research should prioritize external and prospective validation, assessment of clinical utility and patient outcomes, transparent reporting, fairness, regulatory oversight, and effective human–AI integration.
Autosomal dominant tubulointerstitial kidney disease caused by UMOD variants (ADTKD-UMOD) is a rare hereditary disorder characterized by early-onset hyperuricemia, gout, and progressive kidney dysfunction. Diagnosis is established by genetic testing. We report the case of a 25-year-old man who presented with elevated serum creatinine (Scr) and uric acid (UA) levels. His father and elder sister had chronic kidney disease of unknown etiology, suggesting an autosomal dominant inheritance pattern. A comprehensive evaluation excluded secondary causes of hyperuricemia and kidney dysfunction. Genetic testing identified a novel heterozygous missense variant, UMOD (NM_003361.4): c.274T>A (p.Cys92Ser), in exon 3 of the gene. The same variant was also detected in affected relatives. In silico analyses predicted a deleterious effect, and the variant was classified as likely pathogenic according to the ACMG/AMP criteria (PM5_Moderate, PP3_Moderate, PM2_Supporting). During longitudinal follow-up with febuxostat treatment, serum urate levels decreased, while progressive deterioration of renal function was observed during the observational period. By analogy to well-characterized pathogenic cysteine-altering UMOD variants, we hypothesize that p.Cys92Ser may promote uromodulin misfolding and endoplasmic reticulum retention and thereby contribute to kidney injury; this mechanistic inference remains to be verified by direct functional experiments for this novel variant. This report expands the mutational spectrum of ADTKD-UMOD and underscores the importance of early genetic testing in at-risk families, as well as standardized long-term follow-up and management for this progressive disorder.
