Based on many basic studies, primary IgA nephropathy is considered to be caused by the production of underglycosylated IgA1 and autoantibodies directed against such abnormal IgA1 molecules and subsequent immune complex formation and mesangial deposition, leading to glomerular inflammation.[15] Therefore, immune disturbance should play a pivotal role in the pathogenesis of primary IgA nephropathy. This evidence concerns the gene IGHA1 and IgA glomerulonephritis.