The occurrence of IgA nephropathy has significant geographical and ethnographic differences. Although most studies have confirmed that the occurrence and development of the disease are closely related to a variety of factors such as immune dysfunction, infection, and inflammatory response of the body, the above factors alone cannot fully explain the mechanism of the occurrence and development of the disease. Current evidence from many studies indicates that IgA nephropathy is a group of complex diseases with multi-genetic and multifactorial determinants. Among them, genetic factors play an important role in the occurrence and development of the disease. Some investigations found that some patients with IgA nephropathy have obvious family aggregation, and the frequency of abnormally high IgA synthesis in vitro in familial IGA is also more than sporadic, which means that IgA nephropathy is hereditary to some extent. IgA nephropathy is associated with human leukocyte antigens B35, DR4, and B12, indicating the role of heredity in the development of IgA nephropathy. However, some experts believe that IgA nephropathy is not hereditary, only that genetic factors play an important role in the development of IgA nephropathy. IgA nephropathy is mainly caused by infections, the most common of which are mucosal infections, such as pharyngitis, tonsillitis, colds and other upper respiratory tract infections may cause the disease. IgA nephropathy is caused by a variety of factors, that is, people with a genetic predisposition to IgA nephropathy have a defective immune system and are prone to the disease under the influence of repeated inflammatory conditions, such as pharyngitis, tonsillitis, colds and enteritis. Simply put, IgA nephropathy is not a genetic disease, but there is some heritability, which does not mean there is a genetic inevitability. For people who have a family history of IgA nephropathy, one is to have regular health checkups for early detection and timely treatment. Second, we should minimize chronic inflammation and mucosal infections to prevent IgA nephropathy.