Acute Immune Mesangial Injury : a New Model of Glomerulonephritis

A number of experimental immunologic models of glomerulonephritis have been devised in animals in order to better understand mechanisms of immune glomerular injury. From these studies two general pathogenic categories have been defined (1). The first, immune complex injury, involves the interaction of circulating host or foreign antigen with antibody resulting in the formation of soluble complexes that localize in glomeruli, producing injury (2). The second involves the fixation of circulating antibody to host glomerular basement membrane (GBM) l after the passive administration of heterologous anti-GBM antibody (nephrotoxic nephritis) (3), or after the immunization of the host with heterologous or homologous GBM resulting in the production of autologous anti-GBM antibodies (4). Recent evidence has implicated or proved one or the other of these two basic mechanisms to be operative in a variety of human diseases including acute poststreptococcal glomerulonephritis (5), lupus nephropathy (6), glomerulonephritis associated with chronic infection (7), membranous glomerulopathy (8), and Goodpasture's disease (9). However, in many forms of glomerulonephritis seen clinically the role of these mechanisms is uncertain. In at least three diseases, anaphylactoid purpura nephritis, focal glomerulonephritis associated with the syndrome of "benign" recurrent hematuria, and membranoproliferative glomerulonephritis, the primary glomerular pathology occurs in the glomerular mesangium (10).