Mouse malaria nephropathy.
Mice were infected with 1X 107 Plasmodium berghei Yoelii parasites intraperitoneally. Circulating parasite, malaria antibody and C3 concentrations were measures: parasitaemia and hypocomplementaemia were transient, but the antibody response was persistent. Animals were sacrificed at intervals and their kidneys examined: a glomerulonephritis associates with predominantly mesangial deposits of C3, IgG1, IgM and some IgA always developed after 7 days and persisted for up to 6 mth. Malaria antigen and antibody were demonstrated within the glomeruli. Microscopic haematuria occurred with proteinuria but without marked deterioration in renal function. Strains producing high and low affinity antibody were equally susceptible to the disease. Treatment with glucocorticoid, immunosuppressive, platelet function inhibiting and/or anticoagulant drugs, or indomethacin from the 1st day of infection failed to prevent development of the disease or to lead to its early cure. Eradication of the infection within its first 3 days prevented glomerular deposition of antibody and complement, and infection with a smaller antigen load followed by later treatment also produced subsequent cure.
D000818:Animals; D000917:Antibody Formation; D000962:Antimalarials / Q000627:therapeutic use; D003176:Complement C3 / Q000032:analysis; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000473:pathology*; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008288:Malaria / Q000276:immunology / Q000473:pathology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008854:Microscopy, Electron; D010962:Plasmodium berghei; D011507:Proteinuria / Q000209:etiology; D013045:Species Specificity; D013997:Time Factors
D000962:Antimalarials; D003176:Complement C3; D007166:Immunosuppressive Agents; D003404:Creatinine