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Anti–glomerular basement membrane (GBM) disease, characterized by antibodies against the NC1 domain of type IV collagen, presents with rapidly progressive glomerulonephritis that advances quickly to end-stage renal disease if not identified and treated in a timely fashion. Pulmonary involvement, caused by autoantibodies targeting the alveolar basement membrane, occurs in 60% to 80% of patients1 and presents as alveolar hemorrhage. The renal histopathology of anti-GBM glomerulonephritis typically shows a necrotizing and crescentic lesion on light microscopy with linear deposits of IgG along the glomerular basement membrane on immunofluorescence microscopy.
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Jain et al. (2018) studied this question.
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