C3 glomerulopathy (C3G) is a disease caused by abnormal activation of alternative complement pathway, usually by genetic defect of proteins controlling the pathway or antibodies to them. Post-infectious GN (PIGN) is a disease caused by overactivation of alternative complement pathway by bacterial-immunoglobulin immune complex depositing in glomeruli. Before C3 glomerulopathy has been recognized, patients with the disease were diagnosed with atypical PIGN because of similar clinico-pathologic findings.
Al-Ghaithi et al. studied 33 children with PIGN and found almost one fourth of them could be reclassified as C3G. These patients had slow progressive clinical course and lacked classic subepithelial deposits or humps by electron microscopy (EM). Although some PIGN cases showed no IgG staining by immunofluorescence, the humps were identified by EM.
