The pathogenesis of C3G is due to dysregulation of complement alternative pathway (AP) activation which can be acquired (autoantibodies against complement proteins which can be polyclonal or monoclonal, for example, C3 nephritic factors, anti-complement fact H (CFH)) or genetic (e.g., CFH, C3 gene mutations) [1]. This evidence concerns the gene C3 and complement 3 glomerulopathy.