Complement in membranous nephropathy: what we thought we knew and what we really know

Membranous nephropathy (MN), originally called membranous glomerulonephritis, was first described in 1946 by Bell as a glomerular disease characterized by a thickening of the glomerular basement membrane (GBM) and marked proteinuria (Figure 1).1 A series of elegant histopathological analyses and experimental studies in rodents and the isolated perfused kidney system demonstrated that the pathogenesis of this condition involves the deposition of anti-podocyte antibodies in the subepithelial space of the glomeruli, which leads to podocyte injury.