scholarly journals A case of Goodpasture's syndrome presenting with acute renal failure before pulmonary hemorrhage.

2001 ◽  
Vol 34 (8) ◽  
pp. 1205-1210
Author(s):  
Yoshiaki Nishioka ◽  
Yasuhide Kanamoto ◽  
Hiroshige Kawano ◽  
Masanobu Miyazaki ◽  
Takashi Harada ◽  
...  
Nephron ◽  
1991 ◽  
Vol 57 (3) ◽  
pp. 381-382 ◽  
Author(s):  
A. Volpi ◽  
G. Battini ◽  
F. Conte ◽  
G.M. Ferrario ◽  
F. Giordano ◽  
...  

BMJ ◽  
1967 ◽  
Vol 4 (5571) ◽  
pp. 95-95 ◽  
Author(s):  
J F Munro ◽  
A M Geddes ◽  
W L Lamb

2010 ◽  
Vol 49 (14) ◽  
pp. 1401-1403 ◽  
Author(s):  
Yoshikata Morita ◽  
Mako Yasuda ◽  
Mitsushige Nakao ◽  
Yoshinori Tsujimura ◽  
Motohide Isono

2000 ◽  
Vol 191 (5) ◽  
pp. 899-906 ◽  
Author(s):  
Akira Nakamura ◽  
Takae Yuasa ◽  
Azusa Ujike ◽  
Masao Ono ◽  
Toshihiro Nukiwa ◽  
...  

The combination of hemorrhagic pneumonitis and rapidly progressive glomerulonephritis is a characteristic feature of Goodpasture's syndrome (GPS), an autoimmune disease resulting from the interaction of pathogenic anti–collagen type IV (C-IV) antibodies with alveolar and glomerular basement membranes. Lack of a suitable animal model for this fatal disease has hampered both a basic understanding of its etiology and the development of therapeutic strategies. We now report a novel model for GPS using mice deficient in a central regulatory receptor for immunoglobulin (Ig)G antibody expression and function, the type IIB Fc receptor for IgG (FcγRIIB). Mutant mice immunized with bovine C-IV reproducibly develop massive pulmonary hemorrhage with neutrophil and macrophage infiltration and crescentic glomerulonephritis. The distinctive linear, ribbon-like deposition of IgG immune complex seen in GPS was observed along the glomerular and tubulointerstitial membranes of diseased animals. These results highlight the role of FcγRIIB in maintaining tolerance and suggest that it may play a role in the pathogenesis of human GPS.


1991 ◽  
Vol 11 (6) ◽  
pp. 389-397 ◽  
Author(s):  
Douglas E. Roberts ◽  
Carol Peebles ◽  
John G. Curd ◽  
Eng M. Tan ◽  
Robert L. Rubin

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
James Dahlgren ◽  
Marla Wardenburg ◽  
Trevor Peckham

We report a case of Goodpasture's syndrome following chronic low level and an acute, high level of exposure to crystalline silica. A 38-year-old male tilesetter was admitted to the emergency room with dyspnea and respiratory failure. He reported that his symptoms had developed over the previous week after inhaling a large amount of dust while dry-sanding and sweeping a silica-based product used to fill cracks in a cement floor. Over the following days, his pulmonary function declined and he developed acute renal failure. Tests of antiglomerular basement membrane antibody were positive and renal biopsy revealed global glomerulonephritis. He was diagnosed with Goodpasture's syndrome and treated with steroids, plasmapheresis, and hemodialysis. This man had a history of childhood asthma and a remote, one pack-year history of cigarette use. He used the flooring product for seven years prior to the inciting event, however, previous jobs had utilized significantly smaller amounts. Goodpasture's syndrome and other autoimmune diseases have been reported in association with silica exposure. The acute onset following high level silica exposure in this previously healthy man, suggest that clinicians should investigate silica exposure as a causal factor in cases of Goodpasture's syndrome.


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