Association of Low Serum Complement 3 with Worse Glomerular Filtration Rate in Patients with IgA Nephropathy Secondary to Psoriasis

Objective: Complement system is pivotal in the pathogenesis of psoriasis and IgA Nephropathy (IgAN). Few studies have examined the features of patients with IgAN secondary to Psoriasis (IgAN-Pso). The association of serum complement and renal function is unknown. This study was made to investigate the relationship between serum C3 and glomerular filtration rate in patients with IgAN-Pso. Methods: In this retrospective cross-sectional study, eighty-five patients with IgAN without evidence of a secondary cause other than psoriasis were enrolled. Patients were divided into two groups: the serum ≥ 0.9 g/L group (n=56) and the serum <0.9 g/L group (n=29). We used CKD-EPI equation to estimate Glomerular Filtration Rate (eGFR) and Empower Stats software to assess the relationship study. Results: Patients with low serum C3 showed lower eGFR level than those with normal serum C3 (88.7 ml/min/1.73 m2 [57.6-107] and 76.3 ml/min/1.73 m2 [51.2-102]). No statistically differences were found in the histological characteristics between the two groups. Univariate analysis showed a positive correlation between serum C3 and eGFR (β =-26.4, 95%CI: -3.4 to 56.1, P=0.086). After adjusting for confounding factors, the positive correlation between serum C3 and eGFR became statistically significant. The eGFR increased by 7.23 ml/min/1.73 m2 and 7.26 ml/min/1.73 m2 with each increase of 0.1 g/ L of serum C3 in the adjustment II and adjustment III model, respectively. The eGFR in patients with low C3 decreased by 27.8 ml/min/1.73 m2 and 17.2 ml/min/1.73 m2 compared with that in patients with normal C3 levels in the adjustment II and adjustment III model, respectively. Furthermore, curve fitting showed that serum C3 and eGFR had a non-linear positive correlation. Conclusion: Decreased serum C3 was associated with poor renal function in patients with IgAN-Pso, suggesting that complement system could be participated in the pathogenesis of IgAN-Pso.