[A new concept for the pathogenesis of immune complex nephritis]

For a long time it was considered that immune complex nephritis was caused by the deposition of circulating immune complexes. The way these complexes penetrate into the GBM has not been satisfactorily explained. Recently, especially in the case of sub-epithelial immune complex deposits, an in situ formation has been discussed. Positively charged molecules have a marked affinity for the negatively charged GBM and can act as a target (planted antigen) for circulating antibody. Furthermore they can readily penetrate the GBM even when their size exceeds 500,000 daltons, whereas aniocatiocatiocationic molecules of over 70,000 daltons are effectively excluded. The interaction of chemically cationized proteins with the GBM is dependent on the size and charge of the molecule. Cationized IgG fixes to the GBM when its pI exceeds 9.0, ovalbumin only when its pI exceeds 10.0. Highly cationised proteins can be detected for several hours in the GBM. The reaction with antibody leads to the formation of sub-epithelial deposits which persist for weeks or even months in the GBM. Perfusion of microgram quantities of a highly cationised antigen directly into the left renal artery followed by the systemic injection of anti-body 1 h later is capable of inducing a typical ICGN with massive proteinuria. The above demonstrates that cationic proteins are nephritogenic antigens, which may also be involved in human glomerulonephritis.