Immunologic aspects of renal disease.

Abstract

Almost a century and a half ago, Richard Bright suggested that in flammation of the kidney in nephritis was a morbid action directly in­ volving the organ, or a consequence of a morbid action elsewhere, resulting in a deposit in the kidney. After a number of years of intensive investigation in experimental animals and man, we now know that the morbid action is an immunological one, and that the kidney may be damaged by the direct assault of antikidney (glomerular basement membrane) antibodies, or by passive deposition of circulating antigen-antibody complexes in the glo­ merular capillaries. Although there are a number of experimental animal models for the production of acute and chronic glomerulonephritis, the immune injury seems always to be a result of either of th ese two patho­ genetic mechanisms [reviewed in (1)]. As detailed immunopathological studies are made of human glomerulonephritis, clear-cut examples of these mechanisms are being obtained, although a number of cases do not fit a clear-cut pattern of either antikidney antibody disease or complex deposit disease. Most naturally occurring nephritis in man now appears to be of the complex type, but little is known of the qualitative and quantitative aspects of the antigens and antibodies involved in such soluble complex formation. Furthermore, in the less frequently occurring cases due to antiglomerular basement membrane antibody, there are few clues as to why such an auto­ immune process can begin. Both pathogenetic mechanisms can result in either an acute massive inflammatory reaction, or an indolent, slowly pro­ gressing one (2). Regardless of the limitations in our understanding of the unusual anti­ body responses in nephritis, considerable insight has been gained into the proximate causes of inflammation and tissue damage which occur once antibody or antigen-antibody complexes become concentrated in the wall of