Immune Complex Nephritis Induced

Recent experimental studies have shown that the local b inding of circulating ant ibody with antigens existing or planted within the glomerulus can result in damage to this structure (1-6). In particular, chemically cationized proteins are able to bind to the glomerular basement membrane (GBM), act as a planted antigen, and induce in situ immune complex formation accompanied by marked proteinuria (4-6). Negatively charged components in the G B M (7-10) and on the surfaces of endothelial and epithelial cells (11-14) act as a barrier to the passage of anionic, but not cationic macromolecules (15, 16). These fixed anionic sites also function as receptors for cationic substances, and this is the basis of the system developed. We describe the first detailed quanti tat ive studies in a model of in situ immune complex nephritis that uses a cationic antigen, cationized h u m a n immunoglobul in G (IgG). The correlation between the degree of proteinuria and the amount of kidney fixing antigen and ant ibody was investigated. In addition, the distribution of cationized antigen within the organism and the disappearance kinetics of antigen and ant ibody from the kidney were analyzed. The results documented here provide insight into events occurring at a molecular level during immune complex formation involving cationic antigens, which is an essential step before a t tempt ing to extrapolate the concept of charge-based complex localization to man.