C3 and IgA glomerulonephritis: The R102G polymorphism generates the “fast” and “slow” electrophoretic allotypes of C3 (C3F and C3S) [32], showing a differential capacity to bind monocyte-complement receptor C3F [33], which is the risk variant for AMD, and has been previously reported as associated with other immune-mediated conditions, such as IgA nephropathy [34], systemic vasculitis [35], or membranoproliferative glomerulonephritis type II [36].