IGHA1 and IgA glomerulonephritis: Current data indicates that at least four hits contribute to development of IgA nephropathy: aberrant glycosylation of IgA1, synthesis of antibodies directed against galactose-deficient IgA1, binding of the galactose-deficient IgA1 by the anti-glycan/glycopeptides antibodies to form immune complexes (ICs), and accumulation of these complexes in the glomerular mesangium to initiate renal injury[2].