A 56-year-old male admitted to the hospital for generalized weakness and fever. He was treated in hospital for 10 days due to COVID-19. He did not receive any immunosuppressive therapy during admis...

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 and Objectives: Donor acute kidney injury (AKI) is increasingly recognized in deceased-donor kidney transplantation. However, its independent association with long-term graft outcomes remains controversial. We investigated whether donor AKI predicts death-censored graft failure (DCGF) after adjusting for confounding factors and competing risks. Materials and Methods: We conducted a retrospective cohort study of 285 deceased-donor kidney transplant recipients (146 with AKI donors, 139 with non-AKI donors). Propensity score matching (1:1 matching, caliper = 0.2 SD) created 110 matched pairs. The matched pair structure was accounted for in the competing risk regression by specifying robust variance estimation with clustering on matched pairs' IDs. The primary outcome was DCGF, analyzed using competing risk regression (Fine-Gray model) with patient death as a competing event. Secondary outcomes included delayed graft function (DGF), acute rejection, and patient survival. Results: After matching, baseline characteristics were well-balanced (all SMD 14 days (sHR 2.15, p=0.001), acute rejection (sHR 2.45, p<0.001), and expanded criteria donor status (sHR 1.98, p=0.005) were independent predictors of DCGF, while donor AKI severity showed no dose-dependent effect (p=0.586). Conclusions: Donor AKI does not independently predict long-term graft failure when confounding is minimized through propensity score matching and competing risks are appropriately modeled. Post-transplant factors, particularly DGF duration and acute rejection, are the dominant determinants of graft survival. These findings support the selective use of AKI donor kidneys in appropriate recipients and emphasize the importance of post-transplant management strategies, especially monitoring DGF duration.

Background: Early postoperative changes in creatinine-based estimated glomerular filtration rate (eGFR) after bariatric surgery can be misread as a kidney injury. During rapid weight loss, indexing eGFR to a fixed body surface area (BSA) of 1.73 m² may alter apparent trajectories. We compared absolute (mL/min) and BSA-indexed (mL/min/1.73 m²) eGFR changes after sleeve gastrectomy, stratified by baseline glomerular hyperfiltration (GH). Methods: In this retrospective cohort of 145 adults undergoing laparoscopic sleeve gastrectomy, serum creatinine was obtained at baseline (≤30 days pre-op) and 3 months (post-op days 75–105). Indexed eGFR was calculated with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) 2021 creatinine equation; BSA with the Mosteller formula; and absolute eGFR as indexed eGFR × (BSA/1.73). GH was defined as indexed eGFR ≥ 120 mL/min/1.73 m². A REML mixed-effects model (Group, Time, Group × Time) with patient-cluster bootstrap inference was used. An age-adjusted sensitivity model including Age and Age × Time was also fitted. Results: Fifty-four participants (37%) met the GH criteria. Absolute eGFR declined by −26.6 mL/min in GH versus −17.3 mL/min in non-GH (difference-in-differences [DiD] −9.3 mL/min; 95% CI −13.9 to −4.7; p < 0.001). The indexed eGFR changes were smaller (−4.2 vs. −0.5 mL/min/1.73 m²; DiD −3.7; 95% CI −7.3 to −0.03; p = 0.048; bootstrap p_sign = 0.052). In the age-adjusted sensitivity model, the Group × Time interaction for absolute eGFR attenuated but remained statistically significant (−6.57 mL/min; 95% CI, −13.09 to −0.06; p = 0.048), whereas the corresponding interaction for indexed eGFR was attenuated and no longer statistically significant (−3.99 mL/min/1.73 m²; 95% CI −9.15 to 1.16; p = 0.129). Conclusions: Within three months after sleeve gastrectomy, participants with higher baseline indexed filtration showed a larger decline in absolute eGFR but only a small change in indexed eGFR. These results show that early postoperative creatinine-based eGFR trajectories are scale dependent and should be interpreted cautiously during rapid weight loss. Because postoperative acute kidney injury (AKI) was not adjudicated and direct kidney function markers were unavailable, this study does not distinguish physiological hemodynamic change from structural kidney injury. Reporting both absolute and indexed eGFR may improve early postoperative interpretation and help align dosing decisions with rapid changes in body size.