Immunopathologic mechanisms of renal disease

Abstract

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 glomerulonephritides, respectively 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, membranproliferative and rapidly progressive morphologic varieties often accompanied by nephrotic 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.