C5 and glomerulonephritis: Even in vivo models support complement as a key player in the pathogenesis of AAV: complement activation by alternative pathway, in particularly C5aR, is required for the onset of glomerulonephritis (Schreiber et al., 2009; Xing et al., 2009; Xiao et al., 2014), and mouse knocked-out for C5 as well as factor B–but not C4- were protected from disease onset (Noone et al., 2018).