IGHA1 and glomerulosclerosis: The “four-hit hypothesis” of IgAN pathogenesis (Suzuki et al., 2011) involves: elevated serum galactose-deficient IgA1 (Gd-IgA1), IgG or IgA antibodies specific to Gd-IgA1, the formation of immune complexes (ICs), and IC deposits predominantly on the glomerular mesangium, leading to inflammation, complement activation, mesangial hypercellularity, and glomerulosclerosis.