Background: Finerenone has emerged as a promising nonsteroidal mineralocorticoid receptor antagonist for patients with chronic kidney disease (CKD), yet its safety and efficacy in kidney transplant recipients remain unstudied. Methods: A total of 1750 kidney transplant recipients were screened, and 39 were prescribed finerenone alongside angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers. Fifteen patients who met inclusion criteria and used finerenone consistently for at least six months were compared with 15 matched controls. Proteinuria, renal function, serum potassium, and other laboratory and clinical parameters were assessed at baseline and at 1, 3, and 6 months. Results: Finerenone was discontinued in two patients (5.1%) due to flushing and headache. Severe hyperkalemia occurred in four patients (10.2%). In the finerenone group, proteinuria significantly decreased at all time points (p < 0.05), with a 40% reduction at six months. No significant changes in estimated glomerular filtration rate or serum creatinine were observed. Conclusions: Finerenone is a promising adjunct therapy in kidney transplant patients for reducing proteinuria without impairing renal function for those patients who can tolerate it. However, in the early phase of treatment initiation, patients should be closely monitored for adverse effects including hyperkalemia.

Background: Sodium–glucose cotransporter 2 (SGLT2) inhibitors have demonstrated significant renoprotective effects in patients with chronic kidney disease. However, kidney transplant recipients have been excluded from major randomized trials, and evidence in non-diabetic transplant patients remains limited. This study aimed to investigate the potential effects of SGLT2 inhibitors in non-diabetic kidney transplant recipients. Methods: Kidney transplant recipients were screened retrospectively and divided into two groups based on SGLT2 inhibitor use. A total of 18 non-diabetic patients receiving SGLT2 inhibitors (Group 1) were compared with 30 matched controls (Group 2). Patients were followed at baseline, 3, 6, and 12 months. Proteinuria, serum creatinine, eGFR, uric acid, and tacrolimus levels were analyzed. Results: Baseline demographic and biochemical characteristics were similar between groups. In Group 1, proteinuria decreased by 20% at 6 months and 26% at 12 months compared with baseline. The reduction in proteinuria from baseline to 6 months was significantly greater in Group 1 than in controls (p = 0.037). No significant changes were observed in serum creatinine, eGFR, tacrolimus levels, or infection-related adverse events between groups. Conclusions: SGLT2 inhibitors may confer an early antiproteinuric benefit in non-diabetic kidney transplant recipients without apparent adverse effects on renal function or safety. Larger prospective studies are needed to confirm long-term effects.

Background: Cardiovascular disease is a major cause of morbidity and mortality in patients with end-stage kidney disease receiving maintenance hemodialysis. Visfatin is a pro-inflammatory adipokine involved in metabolic and inflammatory pathways; however, its relationship with established coronary artery disease (CAD) in hemodialysis patients remains uncertain. This study evaluated the associations of serum visfatin concentrations with hemodialysis status, clinically documented CAD, and selected metabolic and biochemical parameters. Methods: This cross-sectional study included 130 non-diabetic adults classified into four groups: healthy controls (n = 40), participants with preserved renal function and established CAD (n = 28), maintenance hemodialysis patients without CAD (n = 30), and maintenance hemodialysis patients with established CAD (n = 32). Demographic, anthropometric, and laboratory variables were recorded. Serum visfatin concentrations were measured using an enzyme-linked immunosorbent assay. Between-group comparisons and exploratory correlation analyses were performed. Analysis of covariance was additionally used to assess between-group differences in visfatin after adjustment for age, sex, hypertension, and BMI, with body fat percentage substituted for BMI in a sensitivity analysis. Results: Median serum visfatin concentration was higher in the pooled hemodialysis groups than in the pooled non-hemodialysis groups (35.75 vs. 30.51 ng/mL, p = 0.014). In unadjusted pairwise comparisons, healthy controls had lower visfatin concentrations than participants with preserved renal function and CAD (p = 0.007), hemodialysis patients without CAD (p = 0.001), and hemodialysis patients with CAD (p = 0.004). However, visfatin concentrations did not differ between hemodialysis patients with and without established CAD (p = 0.972). After adjustment for age, sex, hypertension, and BMI, the overall between-group effect was no longer statistically significant (F(3, 122)= 2.054, p = 0.110, partial η² = 0.048). The result was similar in the sensitivity analysis replacing BMI with body fat percentage (p = 0.060). In exploratory analyses of the pooled hemodialysis population, visfatin was positively correlated with fasting insulin (r = 0.269, p = 0.039), HOMA-IR (r = 0.277, p = 0.033), and serum uric acid (r = 0.263, p = 0.039). Conclusions: Higher serum visfatin concentrations were observed in patients receiving maintenance hemodialysis in unadjusted analyses, but the overall between-group difference was attenuated after adjustment for demographic and body-composition variables. Visfatin did not distinguish hemodialysis patients according to established CAD status. These findings do not demonstrate an independent association of circulating visfatin with either hemodialysis status or clinically documented CAD. Given the cross-sectional design and exploratory nature of the correlation analyses, further prospective studies with larger samples and standardized assessment of coronary disease burden are warranted.

Background: Patients with chronic kidney disease (CKD), including autosomal dominant polycystic kidney disease (ADPKD), have been reported to be at higher risk for adverse outcomes during the COVID-19 pandemic. We aimed to obtain the characteristics and outcome data obtained in the follow-up of patients with ADPKD who survived COVID-19 and to compare these data with a control group with ADPKD who were COVID-19 naive. Methods: In this national, multicenter observational study, adult ADPKD patients who survived COVID-19 were included, and ADPKD patients without a history of COVID-19 from the same outpatient clinics were selected as a control group. Baseline characteristics and post-COVID-19 first- and third-month data were recorded. Results: In this study, a total of 72 ADPKD patients from 16 centers were included in the study (COVID-19 group, n: 40, non-COVID-19 control group, n: 32). Fourteen (33.3%) patients in the COVID-19 group were hospitalized during active COVID-19. During the first and third months after COVID-19, none of the patients died in either group. Urinary tract infection was significantly higher in the non-COVID-19 group than in the COVID group in the third month (0% vs. 12.5%, p = 0.021). All other follow-up outcomes, including respiratory symptoms and initiation of kidney replacement therapy (KRT), were not different between the groups in the first and third months. The laboratory data of the groups in the first and third months were not significantly different. Hematuria and leukocyturia ratios were also not statistically significantly different between the groups. Conclusions: ADPKD patients who survive COVID-19 have no worse short-term outcomes than non-COVID-19 ADPKD patients, including respiratory symptoms, initiation of KRT, and death.

Background: Fabry disease may cause clinically silent kidney involvement before marked loss of kidney function. Objectives: To characterize pediatric and adult patients with Fabry disease, focusing on early kidney findings and age-related organ involvement. Methods: This retrospective, single center study included 16 patients followed between 2016 and 2026. GLA variants were identified by targeted next-generation sequencing. Patients were classified as children (≤18 years, n = 7) or adults (>18 years, n = 9) at the final evaluation. Results: Family screening identified 10 of 16 patients from six families. Six of these ten patients had no complaints before diagnosis. The median age at diagnosis was 24.5 years (range, 7–60). In nine patients with known symptom onset, the median onset age was 14 years (range, 8–35), and the diagnostic delay was 8 years (range, 1–30). At baseline, proteinuria was detected in eight (50%), hematuria in seven (43.8%), and hypertension in three patients (18.8%). Children had no hypertension or marked kidney dysfunction, although proteinuria and hematuria were each observed in two. Among adults, proteinuria occurred in six, microscopic hematuria in five, and hypertension in three. Left ventricular hypertrophy and valvular abnormalities occurred only in adults. At the final evaluation, proteinuria was present in 10 patients (62.5%). One adult experienced an estimated glomerular filtration rate decline from 70 to 14 mL/min/1.73 m² and required kidney replacement therapy. Conclusions: The diagnostic delay underscores the value of family screening. At baseline, proteinuria and hematuria were observed in both age groups, whereas hypertension, cardiac abnormalities, and advanced kidney dysfunction were confined to adults. During follow-up, hypertension developed in one pediatric patient. These findings support kidney surveillance from childhood onward.

Background: Primary glomerular diseases (PGDs) are a leading cause of end-stage kidney disease (ESKD). While sex differences in chronic kidney disease progression have been reported, their role in PGDs remains unclear. Methods: We analyzed 2081 patients with biopsy-proven PGDs from the Turkish Society of Nephrology Glomerular Diseases Working Group (TSN-GOLD) registry. Baseline demographic, clinical, biochemical, and histopathological characteristics were compared between women and men. Outcomes were assessed as a composite of ESKD or death. Logistic and Cox regression models were applied to identify independent risk factors. Kaplan–Meier analyses evaluated survival differences. Results: At baseline, women and men had similar rates of hypertension (36.8% vs. 34.7%, p = 0.322). Women more frequently presented with leukocyturia (31.7% vs. 17.2%, p < 0.001) and hematuria (57.8% vs. 52.3%, p = 0.016), whereas men had higher proteinuria (5011 ± 4925 vs. 4388 ± 4529 mg/day, p = 0.003) and were more likely to be active smokers (20.7% vs. 7.4%, p < 0.001). Serum albumin (3.3 ± 0.8 vs. 3.2 ± 0.9 g/dL) and eGFR (79.7 ± 44.3 vs. 78.7 ± 45.5 mL/min/1.73 m²) were comparable between sexes (both NS). During a median follow-up of 24 months (IQR 7-60), 431 patients (20.7%) reached the composite outcome of ESKD or death (137 deaths [6.6%], 294 ESKD [14.1%]). In the multivariable Cox regression model, lower baseline eGFR (HR 0.98, 95% CI 0.98–0.98, p < 0.001), lower serum albumin (HR 0.65, 95% CI 0.55–0.77, p < 0.001), higher proteinuria (HR 1.03, 95% CI 1.00–1.05, p = 0.043), and biopsy diagnosis of RPGN (HR 3.78, 95% CI 1.37–10.45, p = 0.010) were independent predictors of poor prognosis. Sex was not an independent predictor of outcome (p = 0.48). Kaplan–Meier analysis demonstrated no significant survival difference between women and men (log-rank p = 0.052). Conclusions: In this nationwide PGD cohort, women and men differed significantly in baseline biochemical and clinical parameters, yet sex was not independently associated with progression to ESKD or death. Instead, disease severity at baseline and histopathological features were the main drivers of prognosis.