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Goodpasture’s Syndrome

  • Chapter
Therapy of Renal Diseases and Related Disorders

Abstract

Beginning with studies at the turn of the century using crude anti-kidney antisera, anti-glomerular basement membrane (GBM) antibody disease has become the clearest example of antibody-induced glomerular injury (1). In animal studies, it can be clearly shown that glomerular injury produced by anti-GBM antibodies is dose dependent and that temporal features of glomerular binding affect the extent of the inflammatory response and, in turn, the degree of injury induced. The experimental anti-GBM antibody model has been used widely to demonstrate the roles of inflammatory mediators. These mediators include humoral factors such as the complement proteins (both early- and late-acting components) and cellular elements including polymorphonuclear (PMN) leukocytes, monocytes/macrophages, and the enzymatic, oxidative, and other iflammatory elements contained therein (1–3).

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Authors
  1. Curtis B. Wilson
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Editors and Affiliations

  1. Baylor College of Medicine, The Methodist Hospital, Houston, Texas, USA

    Wadi N. Suki

  2. Division of Nephrology, University of Southern California, Los Angeles, California, USA

    Shaul G. Massry

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© 1991 Kluwer Academic Publishers

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Wilson, C.B. (1991). Goodpasture’s Syndrome. In: Suki, W.N., Massry, S.G. (eds) Therapy of Renal Diseases and Related Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0689-4_21

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  • DOI: https://doi.org/10.1007/978-1-4613-0689-4_21

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-8027-9

  • Online ISBN: 978-1-4613-0689-4

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