Induction of an autologous immune-complex glomerulonephritis in the rat by intravenous injection of heterologous anti-rat kidney tubular antibody. I. Production of chronic progressive immune-complex glomerulonephritis.

An autoimmune kidney disease morphologically and functionally similar to the Heymann autoimmune nephrosis can be produced in rats by the injection of BSA followed by heterologous anti-rat kidney tubular antibody. Animals injected with the anti-kidney tubular antibody only, developed a milder form of the typical renal lesion without proteinuria. Control animals injected with BSA or normal rabbit serum alone and BSA and normal rabbit serum together did not develop a progressive type of kidney disease. Gamma-globulin eluted from the developed lesions of the heterologous antibody induced glomerulonephritis was autologous IgG which reacted with the periluminal zone of the proximal tubules on normal rat kidney sections in a fluorescent antibody test. Gamma-globulin eluted from kidneys of homologous renal antigen induced autologous immune complex (AIC) nephritis reacted with normal rat kidney sections in a similar manner. It is suggested that heterologous anti-tubular antibody reaching the proximal convoluted tubules is reabsorbed and releases the nephritogenic antigen with subsequent formation of autoantibody to it. The continuous release of the nephritogenic antigen and the development of the chronic progressive autologous immune-complex glomerulonephritis is maintained by autoantibody produced as the result of the ongoing autoimmune processes.