IGHA1 and infection: The pathogenesis of IgAVN is similar to the “four-hit” hypothesis of IgAN, in which the abnormal immune response of the body is activated by precipitating events such as infection, leading to overproduction of galactose-deficient IgA1 and the formation of an immune complex containing Gd-IgA1, which is then deposited in the kidney and promotes the development of IgAVN.