Helicobacter pylori participates in the pathogenesis of IgA nephropathy.

Increasing evidences have shown that Helicobacter pylori (Hp) is a pathogen closely related to extra-gastric disorders. Our previous in vitro studies had demonstrated that Hp infection, at least via cytotoxin-associated gene A protein (CagA), might play an important role in the pathogenesis of IgA nephropathy (IgAN) by stimulating proliferation and ectopic synthesis of aberrantly glycosylated IgA1 of B cells. However, the relevant clinical evidence of IgAN resulted from Hp infection remain to be elucidated. This study aimed to investigate the risk incidence of IgAN caused by Hp infection. 22 primary IgAN, 20 non-IgA nephropathy (n-IgAN), and 30 healthy controls were included in this study. We found that the rate of IgG anti-Hp seropositivity was significantly improved in IgAN, but the current Hp infection was similar in all groups. The production and underglycosylation of IgA1 tended to increase in IgAN patients with IgG anti-Hp seropositivity. A tendency toward increased the risk of clinical prognosis was seen in IgAN with Hp infection. Hp antigen and CagA were only deposited in renal tubules, and enhanced antigen deposition in response to Hp was observed in IgAN. Our study suggested that Hp infection might have a pathogenic role in IgAN through giving rise to strongly mucosal immune response, and based on damage of renal tubular.