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Background and AimsMesangial C3 deposition is frequently observed in patients with IgA nephropathy (IgAN). However, the role of complement in the pathogenesis or progression of IgAN is uncertain. In this observational cohort study, we aimed to identify the clinical implications of circulating C3 levels and mesangial C3 deposition and to investigate their utility as predictors of renal outcomes in patients with IgAN.MethodsA total of 343 patients with biopsy-proven IgAN were enrolled between January 2000 and December 2008. Decreased serum C3 level (hypoC3) was defined as C3 <90 mg/dl. The study endpoint was end-stage renal disease (ESRD) and a doubling of the baseline serum creatinine (D-SCr).ResultsOf the patients, there were 66 patients (19.2%) with hypoC3. During a mean follow-up of 53.7 months, ESRD occurred in 5 patients (7.6%) with hypoC3 compared with 9 patients (3.2%) with normal C3 levels (P = 0.11). However, 12 patients (18.2%) with hypoC3 reached D-SCr compared with 17 patients (6.1%) with normal C3 levels [Hazard ratio (HR), 3.59; 95% confidence interval (CI), 1.33–10.36; P = 0.018]. In a multivariable model in which serum C3 levels were treated as a continuous variable, hypoC3 significantly predicted renal outcome of D-SCr (per 1 mg/dl increase of C3; HR, 0.95; 95% CI, 0.92–0.99; P = 0.011). The risk of reaching renal outcome was significantly higher in patients with mesangial C3 deposition 2+ to 3+ than in patients without deposition (HR 9.37; 95% CI, 1.10–80.26; P = 0.04).ConclusionsThis study showed that hypoC3 and mesangial C3 deposition were independent risk factors for progression, suggesting that complement activation may play a pathogenic role in patients with IgAN.

Our study demonstrates that RDW could be an additive predictor for all-cause mortality in AKI patients on CRRT treatment in the ICU.

We showed that increased LAVI predicted adverse outcomes better than other echocardiographic parameters in patients with CAPD.

Henöch-Schönlein purpura nephritis (HSPN) is considered a systemic form of immunoglobulin A nephropathy (IgAN). Although these are different pictures of a single disease, there are no studies directly comparing long-term outcomes of these two clinical entities. To clarify this, we studied 120 patients with biopsy-proven HSPN and 1070 patients with IgAN. The primary outcome was the composite of a doubling of baseline serum creatinine, end-stage renal disease, or death. Secondary outcomes included the individual renal outcomes or the rate of decline in estimated glomerular filtration rate. In the unmatched cohort, patients with HSPN had more vasculitic symptoms, more favorable histologic features, and were more commonly treated with steroids than patients with IgAN. The risk of reaching the primary outcome was significantly lower in HSPN patients than patients with IgAN (hazard ratio, 0.67). The 1:2 propensity score matching gave matched pairs of 89 patients with HSPN and 178 patients with IgAN, resulting in no differences in baseline conditions. In this matched cohort, there were no significant differences in reaching the primary and secondary outcomes between the two groups. Thus, after adjustment by propensity score matching, clinical outcomes did not differ between HSPN and IgAN, suggesting the two forms of the same disease have a similar prognosis.