Pulmonary involvement often precedes the onset of nephritis and is the predominant cause of morbidity and mortality. GBM antibodies are not found in normal healthy individuals. Circulating GBM antibodies can be readily detected in the serum of most patients with Goodpasture's syndrome, but the trigger for the formation of these antibodies is unclear. The course of the disease may be dominated by recurrent hemoptysis or life- threatening pulmonary hemorrhage. The renal involvement is frequently progressive over a matter of weeks.
Immediate treatment is necessary before kidney damage is irreversible.
The identification of the disease is often delayed since it is unexpected. Clinical signs such as hemoptysis, the sudden development of anemia, pulmonary opacities, or oliguria are nonspecific. Remission may follow intensive plasmapheresis combined with steroids and cytotoxic agents. Plasma exchange presumably removes both the GBM antibodies responsible for initiating the damage and the secondary circulating mediators. Traditionally, the diagnosis of Goodpasture's syndrome has depended on finding linear deposits of immunoglobulins along the glomerular basement-membrane by direct immunofluorescence microscopy of renal biopsies.