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Nephrol Dial Transplant (1993) 8: 703-710
© 1993 European Renal Association-European Dialysis and Transplant Association

research-article

Antigen size influences the type of glomerular pathology in chronic serum sickness

P. C. W. Hogendoorn1,, E. B. L. van Dorst1, S. H. van der Burg1, J. A. Bruijn, M. R. Daha2, Ph. J. Hoedemaeker1 and G.-J. Fleuren1

1Departments of Pathology University of Leiden The Netherlands 2Departments of Nephrology University of Leiden The Netherlands

Correspondence and offprint requests to: Correspondence and offprint requests to: Pancras C W. Hogendoorn MD PhD, Department of Pathology, University of Leiden, P.O Box 9603, 2300 RC Leiden, The Netherlands.

Chronic serum sickness was induced in four groups of Wistar rats by immunization with BSA, cationized BSA (cBSA), human IgG (HuIgG), or human 1gM (HuIgM), followed by repeated intraperi toneal (i.p.) injection of the antigen used, to study the effect of the characteristics of an antigen on renal immunopathology. Renal tissue sampled 2, 4, 7, and 9 weeks after the start of the i.p. injections was examined by light-, immunofluorescence-, and electron microscopy. Proteinuna was measured in urine col lected over 24 h. All animals given BSA, cBSA, or HuIgG developed progressive renal disease character ized by initial deposition of antigen and rat Ig in the mesangium of rats given BSA or HuIgG, and minimal amounts in those given cBSA, followed by the appear ance in the first instance of subendothelial deposits in the animals receiving BSA or HuIgG, and later subepi thelial deposits in those given BSA, cBSA, or HuIgG. The appearance of immunoglobulin deposits along the glomerular capillary wall was associated with the onset of massive proteinuria reaching average levels of 450 mg/24 h for rats given BSA or cBSA, and 500 mg/24 h for those given HuIgG. Animals injected with HuIgM showed only mesangial deposits of human 1gM and rat Ig without the development of proteinuria. Under light-microscopy, rats given BSA, cBSA, or HuIgM showed minimal abnormalities, whereas those receiving HuIgG showed transient but severe influx of granulocytes in glomeruli with the development of diffuse proliferative glomerulonephritis in association with a long-lasting phase characterized by subendothel ially localized immune aggregates. No differences in the degree or type of the immune response were found either as measured by ELISA or double radial immuno diffusion. We conclude that the type of glomerular immunopathology during chronic serum sickness is partially dependent on the size of the antigen used for induction of the disease.

Keywords: chronic serum sickness; antigen size; ELISA


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