| objective: IgA nephropathy(IgAN) is one of the most common causes of glomerulonephritis in the world. Approximately 30%–50% of patients will develop end-stage renal disease(ESRD) within 20 years of the initial biopsy. Today, Helicobacter pylori(H pylori) infection is a focus of attention, recent studies have suggested that Helicobacter pylori infection may be associated with IgA nephropathy. Our previous in vitro studies have demonstrated that Hp infection, at least via CagA, may participate in the pathogenesis of IgAN by stimulated cell proliferation, influencing the production and glycosylation of IgA1,but the relevant clinical evidence remain absent. The aim of present study is to investigate the clinical evidence of IgA nephropathy resulted from Helicobacter pylori infection. Methods : This study includes 22 patients with primary IgAN and 21 patients with non-IgAN diagnosed from renal biopsy. The healthy population controls consisted of 30 residents of the same geographic area matched by age and gender with the IgAN patients. The carbon 14-urea breath test(14C-UBT)and enzyme-linked immunosorbent assay for the detection of H. pylori IgG antibodies in the serum were performed. The production and glycosylation of IgA1 in patients’ serum were determined by ELISA and helix aspersa(HAA) lectin binding assay, respectively. Immunohistochemistry technique were used to clarify H. Pylori antigen and cytotoxin associated gene A protein(CagA)in renal tissue. Complete clinical data, including age, gender, course of disease, serum creatinine, total serum IgA, complement C3,24-h total protein excretion and estimated glomerular filtration rate(eGFR) were collected at the time of renal biopsy. Results: 1ã€Compare with n-IgAN group and healthy population control group,the H. Pylori infection rate of IgAN group was no differentiation. However, the rate of IgG anti-Hp seropositivity in Ig AN group was significantly greater than n-IgAN group and healthy population control group(P<0.05). 2ã€In IgAN patients, the production and glycosylation of IgA1 was riser in the positive Hp infection patients’ serum. 3ã€In IgAN patients, the total serum IgA and complement C3 was higher in the positive Hp infection patients,24-h total protein excretion and estimated glomerular filtration rate(eGFR) was lower in positive Hp infection patients.4ã€H. Pylori antigen and CagA were consistent deposited in renal tubule,the degree of antigen deposition was obviously enhanced in IgAN patients’ renal tissue. In IgAN patients’ renal tissue, Hp antigen and CagA positivity of H. Pylori infection patients was significantly riser than non-H. Pylori infection patients(P<0.05). Conclusions:The rate of H. Pylori infection was no difference in IgAN group,n-IgAN group and healthy population control group. By inducing strong immune response, H.pylori induced the antibodies against Hp infection increased significantly,promoted the production and underglycosylation of IgA1,and exacerbate the renal function. H. Pylori antigen and CagA were deposited in renal tubule,the degree of antigen deposition was obviously enhanced in IgAN patients’ renal tissue. H. Pylori infection lead to the chance of antigen deposition was increased significantly in IgAN patients. These results suggested that Hp infection may play an important role in the pathogenesis of IgAN,and eradication of Hp infection may be helpful for the treatment of the positive Hp infection IgAN patients. |