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Immunopathologic mechanisms of renal disease

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Ricerca in clinica e in laboratorio

Summary

Anti-GBM antibodies and glomerular deposition of circulating immune complexes are responsible for the immunopathogenesis of about 5 % and 75 % of human glomerulonephritides, respectively. Anti-GBM antibodies most frequently cause rapidly progressive glomerulonephritis accompanied in about half of the patients with pulmonary hemorrhage, the Goodpasture’s syndrome. Immune complexes cause a wide variety of glomerulonephritides, including diffuse and focal proliferative, membranous, membranoproliferative and rapidly progressive morphologic varieties often accompanied by nephrotic syndrome. Immunopathologic tubulo-interstitial renal injury can be caused by antibodies reacting with TBM or by deposition of immune complexes in tubulo-interstitial tissue. Immunofluorescence studies of renal tissue supplemented by detection of circulating anti-basement membrane antibodies and immune complexes are essential in differentiating the immunopathologic mechanisms of glomerular and tubular injury, and are necessary adjuncts in evaluating patients with glomerulo- and tubulo-interstitial nephritis.

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  1. Department of Immunopathology, Scripps Clinic and Research Foundation, 476 Prospect Street, 92037, La Jolla, Calif., USA

    Curtis B. Wilson & Frank J. Dixon

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  1. Curtis B. Wilson
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This is publication No. 876 from the Department of Immunopathology, Scripps Clinic and Research Foundation, 476 Prospect, La Jolla, California 92037. The work was supported in part by United States Public Health Service Contract NO 1-A1-42505 and United States Public Health Service Grant A1-07007.

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Wilson, C.B., Dixon, F.J. Immunopathologic mechanisms of renal disease. La Ricerca Clin. Lab. 5, 17–38 (1975). https://doi.org/10.1007/BF02910013

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