Pathogenesis of anti-basement membrane glomerulopathy and immune-complex glomerulonephritis: dichotomy dissolved

In the last few decades the understanding of pathogenic mechanisms in renal disease has increased considerably. Immunofluorescence studies led to the discovery that most forms of glomerulonephritis in humans are immunologically mediated. Clinically, glomerular diseases are classified on the basis of light and immunofluorescence microscopical patterns, since these provide indications concerning pathogenesis. It has been shown unequivocally that antibodies are involved in the pathogenesis of such diseases as lupus nephritis, membranous nephritis, IgA nephritis, and anti-glomerular basement membrane (GBM) nephritis, but in most cases the pathogenetic antigen involved is not known with certainty. It has become increasingly evident that extracellular matrix and cell-surface antigens can be of pathogenic importance. Recently developed biochemical, immunochemical, and molecular biological techniques open the way to further identification of the pathogenic antigens as well as the mechanisms involved in their interaction with the corresponding antibodies. This paper will analyze recent studies on pathogenic aspects of antiGBM glomerulopathy and immune complex glomerulonephritis. First, etiologic factors are described that are known to operate in animal models of human immunologically mediated glomerulonephritis. Then, a brief review of the earlier work in such animal models is given, followed by a discussion of the meaning of recent observations, which shed new light on existing theories concerning the pathogenesis of immunologically mediated glomerulonephritis