Mucosal immunity plays an important role in the pathogenesis of IgA nephropathy (IgAN). This study aimed to investigate if infection of (), a common bacteria in the gastrointestinal tract, associated with IgAN. This study included 261 patients with IgAN and 46 healthy controls. Clinical information and plasma samples were collected from patients and healthy controls. infection was confirmed by western blot. Plasma IgA1 and galactose-deficient IgA1 (Gd-IgA1) levels were detected by specific enzyme-linked immunosorbent assay. Total infection rates showed no statistical differences between IgAN patients and healthy controls, but the infection rates of type I in IgAN patients were significantly higher than those in healthy controls (44.4 vs. 28.3%,  = 0.040). Compared with uninfected patients, the systolic blood pressure, 24-h proteinuria, and blood urea nitrogen levels were significantly higher in patients with infection (126.0 ± 15.5 vs. 119.6 ± 14.5 mmHg,  = 0.010; 1.8 ± 2.7 vs. 1.2 ± 1.4 g/24h,  = 0.013; 7.9 ± 5.4 vs. 6.7 ± 3.9 μmol/L,  = 0.042), especially in patients with type I infection (126.5 ± 15.4 vs. 119.6 ± 14.5 mmHg,  = 0.002; 1.9 ± 2.9 vs. 1.2 ± 1.4 g/24 h,  = 0.033; 8.1 ± 5.6 vs. 6.7 ± 3.9 μmol/L,  = 0.041). Similarly, patients with IgAN and type I infection showed higher plasma Gd-IgA1 levels than uninfected patients (5.5 ± 2.2 vs. 4.5 ± 2.2 μg/mL,  = 0.037). Virulent type I infection is more common in patients with IgAN. Patients with IgAN and type I infection showed lower renal function and higher underglycosylation of plasma IgA1.