Background: Renal involvement in the diffuse large B-cell lymphoma (DLBCL) is rare and usually occurs as part of systemic disease. Muscle infiltration is even less common and can mimic inflammatory or obstructive conditions. Case presentation: We present a 58-year-old male with right flank pain, myalgia, oliguria, and weight loss. Initial evaluation suggested obstructive nephropathy due to ureteral stones, but renal function did not improve after stone removal. Urine cytology revealed atypical lymphoid cells positive for PAX-5. ¹⁸F-Flourodeoxyglucose Positron Emission Tomography- Magnetic Resonance Imaging (¹⁸F-FDG-PET-MRI) showed pathological ¹⁸F-FDG uptake in the kidneys, multiple muscles, and lymph nodes. Renal biopsy confirmed DLBCL. The patient was treated with daratumumab, rituximab, etoposide, cyclophosphamide, doxorubicin, vincristine, and prednisone, achieving hematologic remission, but remained dialysis-dependent. Conclusion: This case highlights an unusual presentation of secondary renal DLBCL with diffuse muscle involvement, mimicking obstructive acute kidney injury (AKI). The disease should be considered in atypical AKI presentations. Despite systemic treatment response, renal prognosis may be poor in advanced disease.

Background/Objectives: Peritoneal membrane failure remains a major limitation of peritoneal dialysis (PD). Systemic inflammation contributes to membrane dysfunction, yet simple predictive biomarkers are lacking. The uric acid-to-HDL cholesterol ratio (UHR) represents a novel integrative marker of metabolic-inflammatory burden, but its association with membrane failure has not been investigated. Methods: This retrospective cohort study included adult patients who initiated PD between 1997 and 2023. Baseline UHR was calculated from laboratory measurements obtained within the first three months after PD initiation. The primary outcome was peritoneal membrane failure, defined as permanent transfer to hemodialysis due to ultrafiltration failure, inadequate solute clearance, or progressive membrane dysfunction. Receiver operating characteristic, Kaplan–Meier, and Cox regression analyses were used to evaluate the association between UHR and membrane failure. Results: Among 214 patients, 62 (29%) developed membrane failure during follow-up. Baseline UHR was significantly higher in patients with membrane failure. A UHR cut-off value of 14 was identified for risk stratification. In multivariable Cox regression analysis, UHR >14 was independently associated with an increased risk of membrane failure (hazard ratio 1.836, 95% CI 1.040–3.241). A history of kidney transplantation prior to PD initiation also emerged as a strong independent predictor of membrane failure. Conclusions: Elevated baseline UHR is independently associated with peritoneal membrane failure in PD patients. As a simple and readily available biomarker, UHR may support early risk stratification and individualized management. Prospective multicenter studies are warranted to validate these findings.

Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are now foundational therapy for diabetic chronic kidney disease (CKD), yet their ketogenic metabolic effects in this population remain incompletely characterised. While euglycaemic diabetic ketoacidosis is a recognised complication, the prevalence and clinical determinants of subclinical asymptomatic ketonemia in patients with diabetic CKD receiving SGLT-2 inhibitors have not been systematically evaluated. We aimed to determine the prevalence of asymptomatic ketonemia, defined by point-of-care capillary β-hydroxybutyrate (β-HB) positivity, and to identify its independent clinical predictors in this population. This cross-sectional study enrolled 211 consecutive adult outpatients with diabetic CKD receiving SGLT-2 inhibitor therapy (empagliflozin or dapagliflozin). Capillary β-HB was measured under standardised fasting conditions using a point-of-care ketone meter; positivity was defined as β-HB ≥ 0.6 mmol/L. Univariate comparisons were performed using the Mann-Whitney U test, independent-samples t-test, χ² test, or Fisher's exact test as appropriate. Given the low number of outcome events (n = 16), Firth's penalised logistic regression was employed as the primary multivariable analysis to mitigate small-sample bias. Asymptomatic ketonemia was detected in 16 of 211 patients (7.6%), all of whom were clinically asymptomatic at measurement. In Firth's penalised logistic regression, heart failure (OR 4.46; 95% CI 1.48-13.51; p = 0.008), absence of statin use (OR 4.94; 95% CI 1.54-15.86; p = 0.007), and higher HbA1c per 1% increment (OR 1.35; 95% CI 1.01-1.81; p = 0.041) were independent predictors of ketone positivity. Systolic blood pressure showed a borderline inverse association (OR 0.97 per mmHg; 95% CI 0.93-1.00; p = 0.063). No ketone-positive patient was receiving thiazide diuretics (0% vs. 30.3%; p = 0.007). SGLT-2 inhibitor type was not independently associated with ketonemia. Findings were robust on sensitivity analysis with standard logistic regression (Hosmer-Lemeshow p = 0.217; Nagelkerke R²=0.234). Asymptomatic ketonemia is present in approximately one in thirteen outpatients with diabetic CKD receiving SGLT-2 inhibitors. Heart failure, absence of statin therapy, and suboptimal glycemic control independently identify a higher-risk metabolic phenotype, while ketonemia appears unrelated to CKD stage. Although these findings are exploratory and require confirmation in larger prospective studies, they suggest that targeted ketone monitoring may be warranted in selected higher-risk patients.