Background IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide and is an important cause of end-stage renal disease (ESRD). Exploring novel biomarkers is necessary for predicting the disease activity and progression of IgAN patients. The present study sought to investigate the value of serum C4 for predicting the prognosis of IgAN patients. Methods The primary endpoint of this retrospective study was a composite event of either a ≥ 50% reduction in estimated glomerular filtration rate (eGFR) or end-stage renal disease (ESRD) or death. The associations between serum C4 and clinicopathological parameters and prognosis of this cohort of IgAN patients were evaluated. Results The present study included 1356 IgAN patients. Serum C4 levels correlated significantly with clinical prognostic factors. Serum C4 levels correlated positively with urinary protein excretion ( r = 0.307, P < 0.001), and negatively correlated with estimated glomerular filtration rate ( r = − 0.281, P < 0.001). Furthermore, serum C4 levels increased with aggravation of tubulointerstitial injury, crescents and ratios of global sclerosis (all P < 0.05). Prognostic analyses with the Cox proportional hazards regression model and Kaplan-Meier survival curves further identified serum C4 as an independent risk factor for the prognosis of IgAN. Conclusions The present study identified serum C4 as a useful predictor for the prognosis of IgAN patients. The mechanism of the trend of serum C4 in IgAN needs to be illustrated in further research. Electronic supplementary material The online version of this article (10.1186/s12882-019-1420-0) contains supplementary material, which is available to authorized users.
The present study is to establish a nomogram for predicting the prognosis of IgA nephropathy (IgAN). Of the 869 IgAN patients, four-fifths were randomly assigned to the development cohort and one-fifth to the validation cohort. The primary outcome was a composite event of either a ≥ 50% reduction in estimated glomerular filtration rate (eGFR), end-stage renal disease or death. The mean follow-up time was 44 months. The Cox regression model identified urinary protein excretion (1–3.5 g/d, HR 11.639, 95% CI 3.601–37.625; ≥ 3.5 g/d, HR 32.435, 95% CI 10.079–104.380), eGFR (G2, HR 5.293, 95% CI 2.011–13.932; G3, HR 15.797, 95% CI 6.584–37.905; G4, HR 34.619, 95% CI 13.887–86.301; G5, HR 217.651, 95% CI 83.807–565.248), hyperuricaemia (HR 7.031, 95% CI 4.126–11.980), mesangial proliferation (HR 36.667, 95% CI 5.098–263.711), segmental glomerulosclerosis (HR 5.122, 95% CI 3.114–8.425), tubular atrophy/interstitial fibrosis (T1, HR 33.351, 95% CI 7.831–142.044; T2, HR 213.888, 95% CI 51.048–896.182), crescents (C1, HR 3.123, 95% CI 1.771–5.510; C2, HR 7.353, 95% CI 3.590–15.062) and glomerulosclerosis (25–49%, HR 3.123, 95% CI 1.771–5.510; ≥ 50%, HR 14.384, 95% CI 8.813–23.479) for developing the nomogram. The C-index was 0.945 (95% CI 0.914–0.976) in both the development and validation cohorts, showing good agreement between the nomogram-predicted probability and actual free-of-progression probability. Thus, our nomogram could accurately predict the progression of IgAN patients.
The efficacy and safety of mycophenolate mofetil (MMF) for immunoglobulin A nephropathy (IgAN) remains debatable. Therefore, the present meta-analysis was conducted with randomized controlled trials (RCTs). PubMed/MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials were analyzed to identify eligible trials. The pooled risk ratio (RR) with 95% confidence interval (CI) was estimated for all the dichotomous outcome measures. A total of eight RCTs with nine publications (n=510 patients) were included. No significant difference was noted between therapeutic regimens with and without MMF for renal remission and end stage renal disease (ESRD) of patients with IgAN (seven trials; RR, 1.250; 95% CI, 0.993–1.574; P=0.057; and four trials; RR, 0.728; 95% CI, 0.164–3.236; P=0.676). To further define the effects of MMF for renal remission, subgroup analysis was performed, demonstrating that MMF was significantly more effective compared with the placebo (three trials; RR, 2.152; 95% CI, 1.198–3.867; P=0.010), although the immunosuppressive regimens with MMF had no significantly different effects compared with those without MMF (four trials; RR, 1.140; 95% CI, 0.955–1.361; P=0.146), indicating that MMF was superior to placebo and had a similar efficacy to other immunosuppressants for renal remission. In addition, subgroup analysis for ESRD revealed no significant differences between MMF and placebo and between the immunosuppressive regimens with and without MMF (three trials; RR, 0.957; 95% CI, 0.160–5.726; P=0.962; and one trial; RR, 0.205; 95% CI, 0.010–4.200; P=0.303). Furthermore, there were no significant differences between the therapeutic regimens with and without MMF in terms of the risk of adverse events. The present meta-analysis demonstrated that MMF was more effective compared with the placebo, may have similar efficacy to other immunosuppressants in terms of inducing renal remission of IgAN and may not increase the risk of adverse events. The long-term effects of MMF on the prognosis of patients with IgAN require verification in further studies.
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