IGHA1 and IgA glomerulonephritis: The entire process is consistent with the multihit hypothesis of IgA nephropathy, including production of galactose-deficient IgA1 (Gd-IgA1; Hit 1), IgG or IgA autoantibodies that recognize Gd-IgA1 (Hit 2), and their subsequent immune complexes formation (Hit 3) and glomerular deposition (Hit 4), which has been widely supported by many studies.