Rat malarial glomerulonephritis. An experimental model of post-infectious glomerular injury.
This paper describes the immunopathologic findings in acute malaria-associated glomerulonephritis in the rat. Young Sprague-Dawley rats were infected with Plasmodium berghei berghei. The subsequent parasitemia and elevation of circulating Clq-reactive immune complexes were transient while the appearance of anti-plasmodial antibody in the serum was persistent. Sequential examination of renal tissue and urine revealed the following glomerular alterations: (a) granular, predominantly mesangial deposits of IgG, IgM, and C 3, (b) electron dense deposits in the mesangial matrix, (c) glomerular deposition of plasmodial antigen(s) and of anti-plasmodial antibody as demonstrated by acid elution studies, (d) hypercellularity of the glomerular tufts and (e) increased urinary excretion of high molecular weight proteins. All renal abnormalities were transitory, disappearing within one to three months. The results indicate that this form of acute malarial glomerulonephritis in rats is mediated by immune complexes involving plasmodial antigen. The disease resembles the transient glomerular injury complicating cases of Plasmodium falciparum infection in humans. As an easily reproducible model, rat malarial glomerulonephritis appears most suitable for further immunopathologic and functional studies of post-infectious glomerular disease.
D000818:Animals; D000936:Antigen-Antibody Complex; D003176:Complement C3 / Q000032:analysis; D005921:Glomerulonephritis / Q000473:pathology*; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007678:Kidney Glomerulus / Q000032:analysis / Q000648:ultrastructure; D008288:Malaria / Q000473:pathology*; D008854:Microscopy, Electron; D010962:Plasmodium berghei; D051381:Rats; D011919:Rats, Inbred Strains
D000936:Antigen-Antibody Complex; D003176:Complement C3; D007074:Immunoglobulin G; D007075:Immunoglobulin M