ABSTRACT
During the influenza pandemic of 1919, Ernest Goodpasture described an
18-year-old man with fever and cough who developed hemoptysis and renal
failure (1). At autopsy, this patient had histopathological evidence of vasculitis
with focal necrosis within the spleen and intestinal hemorrhage. In 1958, Stanton
and Tange (2) reported a series of men with glomerulonephritis and pulmonary
hemorrhage and designated this constellation of symptoms, Goodpasture’s
syndrome, based on Goodpasture’s earlier report. Subsequent investigations
demonstrated linear deposition of antibodies along the glomerular basement
membrane (GBM) in individuals with Goodpasture’s syndrome and that anti-
bodies eluted from patients’ kidneys induced proliferative glomerulonephritis in
primates (3,4).
