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. 1974 Jun;55(3):282-90.

Induction of an autologous immune complex glomerulonephritis in the rat by intravenous injection of heterologous anti-rat kidney tubular antibody. II. Early glomerular lesions

A Z Barabas, R Lannigan Jr

Induction of an autologous immune complex glomerulonephritis in the rat by intravenous injection of heterologous anti-rat kidney tubular antibody. II. Early glomerular lesions

A Z Barabas et al. Br J Exp Pathol. 1974 Jun.

Abstract

The early effects of a single intravenous injection of anti-rat kidney tubular fraction 3 antibody were studied in rats pretreated with BSA and in untreated animals. Definite deposition of immune complexes, which stained for rat IgG, were noted in the glomeruli of the BSA pretreated rats after one day and in the untreated rats by the fourth day with the fluorescent antibody technique. Control animals injected with normal rabbit serum or BSA and normal controls did not develop immune complex glomerulonephritis. Two of the 4 surviving rats pretreated with BSA and injected with the anti-tubular fraction 3 antibody developed proteinuria towards the fourth week, whereas proteinuria did not occur in the untreated and the control rats.

It is possible that the heterologous anti-rat kidney tubular fraction 3 antibody releases a nephritogenic antigen from the proximal convoluted tubules soon after its administration. Autoantibodies formed are presumably able to form immune complexes with the nephritogenic antigen and produce glomerular injury. As a result of the glomerular damage, the autoantibodies may gain access to the proximal convoluted tubular cells and maintain the release of the nephritogenic antigen.

The developing kidney disease is morphologically similar in every respect to autologous immune complex glomerulonephritis.

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References

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