Mesangial disposal of glomerular immune deposits in acute malarial glomerulonephritis of rats.
The disposal of immune complexes by the glomerulus and the participation of infiltrating monocytes were studied in acute malaria-associated glomerulonephritis. Young Sprague-Dawley rats were infected with Plasmodium berghei. Parasitemia reached a maximum after 8 to 12 days, ending by day 20. In all infected rats, renal immunofluorescence microscopy showed in all glomeruli granular deposition of rat IgG, IgM, and C3 in a mesangial distribution. The staining was strongest from days 8 to 12, then diminished and disappeared after day 32. By contrast, electron-dense deposits were rarely seen before day 16 when they became detectable in the mesangial matrix, particularly along the inner aspect of the glomerular basement membrane. They were most conspicuous on days 20 and 34 and disappeared by day 100. Few monocytes were detected in the glomeruli by electron microscopy and by histochemistry for nonspecific esterase. Highest counts of esterase-positive monocytes were found on day 10 (means 2.9 per glomerulus, range 0 to 5; normal control range 0 to 1). Total glomerular cell counts were transiently elevated on days 10 and 20. Renal functional damage of malarial rats was mild as reflected by a transient increase of urinary protein excretion, whereas serum urea values remained in the normal range. The results suggest that elimination of glomerular immune deposits in acute malarial glomerulonephritis of rats involves their gradual condensation and degradation in the mesangium which reduces detection by immunofluorescence while leading to formation of transient electron-dense deposits. In this model, the efficient disposal of glomerular immune deposits by the mesangium appears to minimize the infiltration of monocytes and to prevent aggravation of the glomerular injury.
D000818:Animals; D000936:Antigen-Antibody Complex; D001485:Basement Membrane / Q000276:immunology; D003176:Complement C3 / Q000032:analysis; D004950:Esterases / Q000032:analysis; D005260:Female; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000209:etiology / Q000473:pathology*; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007678:Kidney Glomerulus / Q000276:immunology*; D008288:Malaria / Q000150:complications* / Q000276:immunology; D008854:Microscopy, Electron; D010962:Plasmodium berghei / Q000276:immunology; D051381:Rats; D011919:Rats, Inbred Strains
D000936:Antigen-Antibody Complex; D003176:Complement C3; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D004950:Esterases