[In situ immune complex glomerulonephritis induced by perfusion of cationized antibody].

In situ immune complex glomerulonephritis can be induced in the rat employing cationized antigen planted in the glomerular basement membrane (GBM) as a target for specific antibody. Another possible mechanism of in situ immune complex formation is antibody already present in the GBM to bind circulating antigen. Present study was performed in order to determine whether cationized antibodies planted in the GBM could react with anionic as well as cationic antigens to form immune deposits. Horse ferritin, rabbit antibody to horse native ferritin (f-Ab) and rabbit antibody to ovalbumin (o-Ab) were highly cationized as described by Danon et al. The ability of the cationized antibodies to precipitate antigens was estimated by Ouchterlony analysis. 500 micrograms/100 g body weight (b.w.) of cationized f-Ab or o-Ab was perfused into the left renal artery of male Wistar rats and 0.1-10.0 mg/100 g b.w. of either native or cationized ferritin or ovalbumin was injected respectively into the tail vein 1 hr later. Estimation of proteinuria was done and the kidneys were removed up to 5 days for immunohistological as well as electron microscopical examination. Cationized antibodies bound to anionic sites of the GBM and combined with subsequently injected cationized ferritin or native ovalbumin in situ, both leading to formation of subepithelial immune deposit with activation of C3 and caused mild proteinuria. Native ferritin, however, induced neither subepithelial immune deposit nor proteinuria, because it didn't permeate through the GBM. The presented model indicates that antibody molecules of high positive charge can bind to the GBM and react with specific antigens that are traversing the barrier to form immune deposits. This is independent of the charge of antigen provided that the antigen molecules are permeable into the GBM, as is the case with ovalbumin but not native ferritin.