The pathogenesis of Goodpasture syndrome includes the presence of autoantibodies directed against the glomerular and/or alveolar basement membrane. As with many autoimmune conditions, the precise cause of Goodpasture’s Syndrome is not yet known. It is believed to be a type II hypersensitivity reaction to Goodpasture’s antigens on the cells of the glomeruli of the kidneys and the pulmonary alveoli. The basement membrane (including a triple chain type IV collagen) lining the alveoli and glomeruli is particularly damaged in patients suffering from Goodpasture syndrome. The immune system misreads self-tissues as foreign, which leads to attack and destruction, as it would happen in case of an invading pathogen. The target antigen that is associated with the strongest pathogenic effect in anti-GBM disease is the non-collagenous 1 domain of alpha-3 type IV collagen. There is strong correlation of anti-glomerular basement membrane disease with allele HLA DRB1-1501. This allele is associated with renal injury. On gross pathology, Goodpasture syndrome with lung involvement may present with diffuse pulmonary hemorrhage. On microscopic histopathological analysis, early focal proliferative changes that display necrosis and crescent formation (due to hypercellular glomeruli) with an inflamed interstitium are seen. Under direct immunofluorescence,  linear immunoglobulin G deposits are found encompassing the glomerular basement membrane and at times the distal tubular portion of the basement membrane.
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