ANCA-associated glomerulonephritis (ANCA-GN) is a leading cause of pauci-immune crescentic GN. Recent evidence indicates that complement activation, marked by C3 deposition in glomeruli, may contribute to more severe renal injury and influence renal outcomes. We aim to evaluate the clinical, histopathological, and prognostic implications of C3 deposition in ANCA-GN. We retrospectively analyzed 195 patients with biopsy-proven ANCA-GN from the Turkish Society of Nephrology Glomerular Diseases registry from 2002 to 2022. Patients were classified as C3-positive or C3-negative according to kidney biopsy immunofluorescence findings. Clinical characteristics, histopathologic lesion profiles, and follow-up outcomes (remission, relapse, and survival) were compared between the two groups. Of 195 patients, 54 (27.7%) had C3 deposition. The C3-negative group was more likely to exhibit PR3-ANCA positivity, whereas the C3-positive group was strongly associated with the presence of MPO-ANCAs (22.2% vs. 77.8%; p = 0.001). Compared with C3-negative patients, C3-positive patients had higher levels of proteinuria (2026 mg/day vs. 1790 mg/day; p = 0.049) and lower HDL levels (30 mg/dL vs. 37 mg/dL; p = 0.009). Fibrocellular crescents were more common in C3-positive patients than in C3-negative patients (p < 0.001). Immune complex deposits, including IgG (26.4% vs. 3.5%; p < 0.001), IgA (14.8% vs. 0.7%; p < 0.001), IgM (25.0% vs. 3.5%; p < 0.001), and C1q (13.7% vs. 0.8%; p < 0.001) were significantly greater in the C3-positive group. However, no significant difference was detected in overall survival (85.8% for C3-negative patients vs. 88.9% for C3-positive patients; p = 0.249). Similarly, the remission (62.1% vs. 59.4%; p = 0.786) and relapse rates (14.8% vs. 11.1%; p = 0.532) did not differ between the groups. In ANCA-GN, glomerular C3 deposition is associated with an MPO-ANCA serotype, greater proteinuria, and more severe renal histology (including immune-complex deposition and more fibrocellular crescents), indicating more pronounced complement activation and tissue injury. However, C3 deposition did not predict worse patient or renal survival in our cohort. Not applicable.

Background Immunoglobulin A nephropathy (IgAN) is a common primary glomerulonephropathy. There is evidence that mesangial C3 deposition plays a role in the development of the disease. The aim of this study was to examine the effect of C3 deposition on the prognosis of IgAN patients. Method The study included 1135 patients with biopsy-confirmed IgAN from the database of the Turkish Nephrology Association Glomerular Diseases Working Group (TSN-GOLD). Patients were excluded from the study if they were aged < 18 or > 75 years or if C3 staining had not been performed in the immunofluorescent analysis. C3 deposition was defined as an immunofluorescence intensity of C3 ≥ 2 + within the mesangium. The primary endpoints were the development of end-stage renal disease, a 30% decrease in glomerular filtration rate compared to the basal value or an elevation in proteinuria to a nephrotic level (3.5 gr/day). Results Mesangial C3 deposition was observed in 603 (53.1%) patients. No statistically significant difference was found at baseline between the groups with and without mesangial C3 deposition, as for age, sex, BMI, proteinuria level, or the presence of hypertension. In the follow-up period with a mean duration of 78 months, no significant difference was found between the two groups regarding the primary endpoints (p = 0.43). A significant correlation between C3 deposition and segmental glomerulosclerosis (S1) according to the Oxford MEST-C classification was found (p = 0.001). Conclusion Although a correlation was observed between mesangial C3 deposition and the S1 MEST-C classification, mesangial C3 deposition was not a prognostic factor in IgAN. Graphical abstract

Objective: BK virus (BKV) infection is a significant concern for kidney transplantation (KT) recipients, potentially leading to nephropathy and graft loss, particularly under intensive immunosuppression. This study investigates the prevalence of BKV infection and its associated risk factors following KT. Materials and Methods: We conducted a retrospective cohort study on 322 KT recipients undergoing routine follow-up in our unit. BKV infection was defined as either high-level BK viruria (BKV DNA load in urine ≥10⁷ copies/mL) or BKV-associated nephropathy. Risk factors were assessed using univariate and multivariate Cox regression analyses. Results: BKV infection was diagnosed in 9.6% (n=31) of patients, with a median onset of 8.7 months (range: 3.02–31.4). Recipients with BK virus infection were more likely to have received kidneys from non-relative living donors (p=0.005). Smoking and calcineurin inhibitor treatment were more prevalent among infected patients compared to those without BKV infection (p=0.015 and p=0.034, respectively). Additionally, BKV-infected patients experienced higher rates of acute rejection episodes (p=0.009) and all-cause allograft loss (p=0.009). In univariate analysis, smoking (hazard ratio [HR]: 2.697, p=0.007), diabetes mellitus (HR: 2.207, p=0.082), non-relative living donors (HR: 4.355, p=0.001), and induction therapy with anti-thymocyte globulin (ATG) (HR: 2.146, p=0.082) were identified as potential risk factors for infection. Smoking and non-relative living donors were independent risk factors for BKV infection (HR: 2.100, p=0.046 and HR: 4.243, p=0.019, respectively). Conclusion: While immunosuppressive therapy is a well-recognized risk factor for BKV infection, our study highlights smoking and non-relative living donors as independent risk factors. Close monitoring of high-risk recipients and smoking cessation counseling should be prioritized to mitigate BKV infection risk.

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.