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/Objectives: Living kidney donors (LKDs) can be at risk of chronic kidney disease (CKD). Several conditions are associated with hyperfiltration, such as solitary kidney, obesity, and high protein consumption. In this regard, we aimed to evaluate the risk factors for kidney function decline in LKDs and the effect of daily protein intake. Methods: Data collected from 220 living kidney donors (mean age: 48.35 ± 12.4 years; 55% female) between 2016 and 2023 were evaluated. One-year and long-term outcomes were evaluated following donor nephrectomy, along with the risk factors for GFR decline and the development of CKD. Results: The percentage of eGFR decline was 31.15 (IQR: 19.81–37.5) in the first year and 28.18 (IQR: 18.75–38.16) in the third year after donation. None of the donors had end-stage renal disease during the 31 (IQR: 19–71) months. CKD developed in 31 (23.1%) LKDs. In the first year, the risk factors associated with a decline in eGFR exceeding 30% included male gender (OR: 0.25; 95% CI: 0.11–0.57; p: 0.001) and baseline eGFR value (OR: 0.95; 95% CI: 0.92–0.98; p: 0.002). At the final visit, the risk factors were male gender (OR: 7.19; 95% CI: 3.06–16.94; p < 0.001), age (OR: 1.06; 95% CI: 1.02–1.10; p: 0.001), and BMI (OR: 1.12; 95% CI: 1.01–1.23; p: 0.030). For the development of CKD, the risk factors were male gender (OR: 0.25; 95% CI: 0.09–0.71; p: 0.009) and baseline eGFR (OR: 0.88; 95% CI: 0.83–0.93; p < 0.001). No association was observed between daily protein intake and renal outcomes in LKDs following donor nephrectomy. Conclusions: In the present study, there was no significant unexpected decline in kidney function in donors in the short-term and the medium-term. Age, BMI, and low basal eGFR values should be carefully considered for LKD evaluation. Furthermore, our findings indicated that protein intake does not substantially impact the GFR. Further controlled studies are required to support our findings.

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

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.

Psoriasis is a chronic, recurrent, inflammatory and common skin disease of unknown aetiology. Amyloidosis is defined as a heterogeneous group of diseases in which generally soluble plasma proteins accumulate in the extracellular space as insoluble abnormal fibrils. Type AA amyloidosis is a late and severe complication of chronic inflammatory disorders and some chronic infections. Although psoriasis is a common inflammatory skin disease, the development of amyloidosis is rare. Herein, we presented a case of psoriasis who developed AA-type amyloidosis.

Background/Objectives: Early death (ED) remains the primary barrier to long-term survival in acute promyelocytic leukemia (APL). Since current risk stratification models rely solely on static baseline parameters, they fail to capture the high biological volatility during the induction phase. We aimed to evaluate the prognostic value of the dynamic evolution of the endothelial activation and stress index (EASIX). Materials and Methods: This multicenter, retrospective study analyzed 131 newly diagnosed adult APL patients treated with the AIDA protocol. EASIX scores were calculated at admission (D0) and day 7 (D7). ROC, landmark, multivariable logistic and Cox regression analyses were performed to assess the impact of dynamic endothelial changes (ΔEASIX) on mortality and survival. Results: The ED rate was 25.2%. While baseline EASIX successfully predicted very early death ( 0.35) was an independent predictor of early mortality (OR: 12.41, p = 0.007), inferior EFS (HR: 5.70, p = 0.004), and poor OS (HR: 3.69, p = 0.023). Landmark analysis stratified by the kinetic trajectory of ∆EASIX confirmed that patients above the optimal cut-off had significantly inferior 3-year EFS (56.3% vs. 77.8%, p = 0.041) and OS (59.5% vs. 78.0%, p = 0.026). Conclusions: To our knowledge, this is the first study to establish EASIX as a dynamic prognostic marker in APL. Our findings indicate that the “kinetic trajectory” of endothelial stress is a more accurate predictor of survival than static baseline assessment alone. While dynamic EASIX monitoring offers a valuable tool for real-time risk reclassification, these results require validation through prospective studies.