Autoreactive B cells produce antibodies against self-antigens, which in native GBM are sequestered within the quaternary structure of the noncollagenous domains of the triple helix of alpha 3,4,5 chains.[9] Subsequently, glomerular injury occurs through complement activation by the classical pathway, IgG Fc receptor (FcγR) mediated phagocytosis or by direct T-cell-mediated toxicity.[10] Anti GBM-GN typically presents with rapidly progressive glomerulonephritis with or without pulmonary hemorrhage. This evidence concerns the gene FCGR2A and Pulmonary hemorrhage.