IGHA1 and nephritis: IgA nephropathy is widely accepted to be a consequence of four hits: circulating IgA1 bearing galactose-deficient O-glycans (Gd-IgA1) in patients with IgA nephropathy is increased (hit 1), and these IgA1 glycobodies are recognized as autoantigens by antiglycan autoantibodies (anti-Gd-IgA1 autoantibodies; hit 2), which leads to the formation of an immune complex in nephritis (hit 3), some of which is deposited in the kidney and activates mesangial cells (hit 4), resulting in kidney injury [34].