The amounts of BSA (immune complex) deposited in glomeruli of rabbits with acute and chronic serum sickness were determined using radio-labeled BSA and paired-label RSA. In animals with acute serum sickness and severe glomerulonephritis, about 18 µg of I*BSA were present in both kidneys after immune elimination (>99% of the circulating I*BSA). Visible with an immunofluorescent sensitivity of 0.25 µg per g of kidney, the I*BSA became rapidly undetectable and was presumably covered by deposits of circulating host anti-BSA and complement which increased demonstrably.

In chronic serum sickness produced by daily injections of a quantity of BSA to balance antibody production, 0.04% of the daily dose of I*BSA was deposited in the glomeruli during the developmental stages of glomerulonephritis. Coincident with the onset of overt proteinuric glomerulonephritis, the daily I*BSA deposition, rate increased to about 0.5% of the daily dose. The half-disappearance rate of I*BSA from the kidney was about 5 days. Administration of huge excesses of BSA caused a fivefold increase in the half-disappearance rate. The accelerated I*BSA disappearance could be correlated with vanishing glomerular immunofluorescent deposits of BSA and immunoglobulin, as well as electron microscopic dense deposits; however, functional improvement of the disease was not observed.

The roles of immune complex size, precipitating and nonprecipitating (total ABC) antibodies, and RES function in the development of chronic serum sickness glomerulonephritis are discussed.

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