Blood purification plays an important role in the treatment of severe acute pancreatitis. Extracorporeal blood anticoagulation is an important strategy to achieve smooth circulation in blood purification circuits. We aimed to investigate the efficacy, safety, and impact on circulating cytokines of using heparin or nafamostat mesylate anticoagulation in patients with severe acute pancreatitis during continuous renal replacement therapy.

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. Hematologic malignancies are known precipitants of disseminated intravascular coagulation (DIC), and the coexistence of these conditions is associated with poor outcomes; however, large-scale data specifically examining concurrent DLBCL and DIC are limited. We performed a retrospective cohort study using the National Inpatient Sample (NIS) to evaluate in-hospital mortality among adult hospitalizations with DIC and/or DLBCL identified using ICD-10 codes. Adults aged ≥ 18 years with a diagnosis of DLBCL and/or DIC were included. In-hospital mortality among patients with concurrent DLBCL and DIC was 54.1%, significantly higher than mortality observed in patients with either condition alone (p < 0.001). In multivariable analysis restricted to patients with both DLBCL and DIC, independent predictors of increased mortality included HIV/AIDS (aOR 4.266, 95% CI: 1.886-9.649; p < 0.001), septic shock (aOR 3.201, 95% CI: 2.305-4.443; p < 0.001), mechanical ventilation (aOR 2.948, 95% CI: 2.175-3.995; p < 0.001), vasopressor use (aOR 2.759, 95% CI: 1.789-4.255; p < 0.001), chronic kidney disease (aOR 2.523, 95% CI: 1.596-3.989; p < 0.001), acute kidney injury (aOR 1.884, 95% CI: 1.347-2.637; p < 0.001), Black race (aOR 2.221, 95% CI: 1.418-3.477; p < 0.001), and Asian or Pacific Islander race (aOR 2.383, 95% CI: 1.329-4.271; p = 0.004) compared to White patients. Bleeding events, thromboembolic complications, stem cell transplantation, and CAR-T therapy were not independently associated with mortality. These findings demonstrate that among patients with DLBCL, the development of DIC is associated with markedly elevated in-hospital mortality, driven predominantly by critical illness, organ dysfunction, and comorbidity burden rather than bleeding or thrombosis alone. Racial disparities in outcomes were independently observed after adjusting for illness severity and comorbidities, warranting further investigation. Early recognition of DIC in patients with DLBCL and aggressive management of systemic complications, particularly septic shock, respiratory failure, and renal dysfunction, may help mitigate disease severity and improve outcomes.

Renal disease in people living with HIV extends beyond classical HIV-associated nephropathy to include immune-mediated and vasculitic lesions, of which pauci-immune crescentic glomerulonephritis is among the rarest and most easily missed. We describe two biopsy-proven cases with anti-myeloperoxidase anti-neutrophil cytoplasmic antibody positivity. The first, established on antiretroviral therapy, presented with a pulmonary-renal syndrome after empirical anti-tubercular treatment had failed; biopsy showed cellular crescents without chronic change, and corticosteroids with rituximab achieved sustained clinical, biochemical and serological remission. The second, antiretroviral-naive, had glomerular haematuria and proteinuria documented at HIV diagnosis and an ischaemic stroke soon afterwards, but declined nephrological assessment; biopsy 3 years later was dominated by global glomerulosclerosis and interstitial fibrosis and he remained dialysis-dependent. The divergence turned on the histological stage at diagnosis rather than antiretroviral status and argues for early biopsy whenever unexplained renal decline with an active urinary sediment occurs in HIV.

In both clinical research and study design, the definition of outcomes for chronic kidney disease (CKD) is changing. New molecules available for testing in humans, and the fact that kidney diseases are best treated earlier in their course, make the duration of studies requiring 'hard endpoints' longer than is feasible for registration purposes and funding agencies. Improved mathematical modelling and statistical analyses, and the availability of electronic medical records and registries have also impacted nephrology clinical research. Thus, eGFR slopes have been promoted as surrogate endpoints for kidney failure, competing-risk methods have exposed the limitations of standard survival analysis in high-mortality CKD and dialysis populations, and pragmatic, registry-based trials enroll patients who resemble those seen in daily practice. This review suggests that eGFR slopes, time to kidney failure, and competing risk factors must be considered in their totality, so that CKD and cardiovascular (CV) evidence can be understood in clinical practice by patients and clinicians. We propose that eGFR slopes may provide a clinically intuitive summary of 'kidney time', showing how, under appropriate conditions, chronic slope differences may be translated into approximate 'years of dialysis delayed' at the population level. We frame competing risks as a clinical, not only statistical, issue, and we examine how pragmatic CKD trials can and should integrate slope-based endpoints and competing-risk analyses into their design and reporting. To advance nephrology research, we must embrace these changes in study design and methodology to ensure that clinicians and patients understand them, and thus are more prepared to implement trial results.

In type 2 diabetes (T2D), kidney fibrosis drives the progression of chronic kidney disease (CKD) and kidney failure. Lower urinary levels of collagen type III degradation (C3M), a biomarker of extracellular matrix (ECM) turnover, have been associated with CKD progression. We investigated the effect of combination therapy with renin-angiotensin system inhibition (RASi) and glucagon-like peptide-1 receptor agonist (GLP-1 RA) on urinary C3M levels in people with T2D. Urinary C3M was measured using the nordicC3M™ ELISA in 229 participants from the Drug Combinations for Rewriting Trajectories of Renal Pathologies in T2D (DC-ren) project. Longitudinal changes in urinary C3M were analyzed using linear regression stratified by treatment group. Risk of kidney disease progression according to baseline urinary C3M was evaluated using Kaplan-Meier analysis. The kidney endpoint was defined as >10% decline in eGFR to <60 ml/min/1.73 m2. Combination therapy (RASi + GLP-1 RA) was associated with higher urinary C3M levels compared with RASi monotherapy (P = 0.036). Urinary C3M was positively associated with future eGFR, with a steeper slope in the combination therapy group than in the RASi monotherapy group (P < 0.001). Low baseline urinary C3M was associated with a higher risk of kidney disease progression (P = 0.022). In people with T2D receiving combination therapy with RASi + GLP-1 RA, urinary C3M levels remained stable, whereas levels decreased with RASi monotherapy, suggesting altered kidney ECM turnover.

Endovascular therapy for occlusive lesion might reduce cardiac afterload and improve cardiac function potentially, but there is limited evidence regarding its effects on heart failure, particularly in patients with poorly controlled symptoms. One month earlier, this 80-year-old woman with paroxysmal atrial fibrillation had undergone left axillo-bifemoral bypass for acute aortoiliac occlusion and was transferred to a rehabilitation hospital. After that, she was returned to our hospital after developing palpitations, dyspnea, and hypoxia during post-operative rehabilitation. Laboratory tests showed anemia, mild renal dysfunction, and markedly elevated B type natriuretic peptide. Chest radiography demonstrated bilateral pulmonary congestion. She was diagnosed to acute heart failure, and treatment with intravenous furosemide at a dose of 40 mg/day and oral amiodarone at a dose of 100 mg/day was initiated. Because sinus rhythm could not be maintained despite medical therapy and pulmonary vein isolation, atrioventricular node radiofrequency catheter ablation and cardiac resynchronization therapy pacemaker implantation were performed on hospital Day 12. However, exertional oxygen desaturation persisted, BNP remained elevated, and rehabilitation was limited by bilateral intermittent claudication. On hospital Day 22, endovascular therapy for aortoiliac occlusive disease was performed. Subsequently, additional endovascular therapy was undertaken for chronic total occlusion of the left superficial femoral artery. She was able to ambulate 20 m with support without any intermittent claudication (ankle-brachial index increased from 0.67 to 0.91 on the right and from 0.81 to 0.98 on the left). Oxygen demand also gradually decreased (from 1 L/min to room air), and B type natriuretic peptide levels declined. Both systolic and diastolic blood pressure improved, and the patient was transferred back to the rehabilitation hospital on hospital Day 54 (32 days after endovascular therapy) without recurrence of heart failure symptoms. This case highlights two clinically relevant points. First, endovascular therapy for aortoiliac occlusive disease led to improvement in heart failure status. Second, B type natriuretic peptide levels showed a clear improvement following endovascular therapy.

Acute kidney injury (AKI) is a common and potentially serious complication, yet population-level data on its burden and determinants remain limited. We quantified AKI incidence, temporal trends, and risk factors across a complete healthcare system. We conducted a population-based cohort study including all adult residents of Stockholm, Sweden (2017-2021) using the SCREAM project. AKI events requiring hospitalization or occurring during hospital stays were identified using a composite algorithm incorporating laboratory-based KDIGO creatinine criteria, ICD-10 diagnoses, and acute dialysis procedure codes. We calculated annual incidence rates, temporal trends using Poisson regression, and incidence rate ratios for selected demographic, clinical, and laboratory-defined risk factors. Among approximately 1.9 million adults annually, 0.6-0.7% experienced AKI each year (71-95 per 10,000 person-years). AKI occurred in 5.8-7.8% of hospitalizations, with only 30% reaching KDIGO stage 2-3. From 2017 to 2021, AKI incidence increased by 26% (95% CI 1.23-1.29). Populations at highest risk of AKI were largely consistent over the years, and included older adults, men, and individuals with uncontrolled diabetes, prior AKI, hypertension, heart failure, kidney transplantation, and multiple myeloma. Lower eGFR and higher albuminuria were associated with markedly higher AKI risk in a graded manner. COVID-19 infection was associated with a six-fold higher AKI risk in 2020, but marked attenuation in 2021 suggests it does not explain the overall upward trend. This region-wide analysis quantifies the contemporary burden of AKI and identifies high-risk populations that may benefit from targeted prevention and monitoring strategies.