A Mini-Epidemic of Goodpasture’s Syndrome

Abstract

Four patients who developed symptoms of Goodpasture’s syndrome during the winter 1971–1972 from a geographic area of about a 25mile radius have been studied. There was an epidemiological association between these cases and a concurrent outbreak of influenza A₂; however, corroborative virologic or serologic evidence could not be obtained. All patients had typical clinical manifestations of severe pulmonary and renal disease. Immunofluorescence studies revealed linear deposits of IgG in all glomeruli studied. C3 was present in three of the four in a granular pattern. Properdin was present in one and C4 in each of the three patients studied.

Anti-glomerular basement membrane glomerulonephritis following nintedanib for idiopathic pulmonary fibrosis: a case report

“…Anti-GBM disease is reported to have the highest rate of crescentic glomeruli at the time of diagnosis [ 4 ]. While environmental factors have been suspected to play a role in the pathogenesis others have reported infection as an inciting factor; however, no clear infective pathogenic association has been identified [ 5 , 6 ]. Multiple case reports also suggest a possible link between hydrocarbon exposures [ 7 , 8 ].…”

Pathogenesis of an experimental model of Goodpasture's hemorrhagic pneumonitis.

“…We tested the effects of IL-2 and IFN-a because Puri and Rosenberg have shown that the association of IL-2 and IFN-a induces in mice the most severe vascular leak syndrome in the lung, whereas IFN-'y and tumor necrosis factor-a do not exert a similar effect when given alone, nor act synergistically with IL-2 (1 1). Moreover, the use of IFN-a was motivated by the consideration that epidemic (26,27) or sporadic (28) outbreaks of influenza or other acute infections (2) have been traditionally associated with Goodpasture's hemorrhagic pneumonitis, and IFN-a is induced by viral infection (29).…”

A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

“…Eleven patients were found to participate in this study. For each of these patients, we retrospectively determined clinical features including age at diagnosis of hydronephrosis, sex, medical history of preexisting renal disease, especially membranous nephropathy, causes of hydronephrosis and the presence or absence of clinical risk factors for the development of anti-GBM antibodies such as smoking history, exposure to organic solvents, recent infection prior to the onset of renal impairment and enforcement of ESWL [ 4 , 5 , 6 , 7 , 10 ]. We also investigated their serum creatinine (sCr mg/dl), the degree of hematuria shown as the number of urinary red blood cells (RBCs) per high-power field (HPF), the deformity of urinary RBCs and RBC cast formation and titer of serum anti-GBM antibodies before and after treatment for hydronephrosis.…”

“…Considering the available evidence, it is hypothesized that a disruption of the stabilized NC1 hexamer and exposure of the cryptic antigen of the α3-chain to the host immune system are required for the development of anti-GBM antibodies [ 3 ]. Several studies have proposed causes for the modifications of intact NC1, namely smoking, infections, exposure to organic solvent and enforcement of extracorporeal shock wave lithotripsy (ESWL) [ 4 , 5 , 6 , 7 ].…”