Abstract
Rabbits experimentally infected with Trypanosoma brucei S42 develop two significant renal lesions: an early proliferative glomerulonephritis associated with glomerular deposits of IgG, IgM, and β 1C laid down in a granular pattern in the glomerular capillary wall as revealed by immunofluorescence, and tubular atrophy with changes in enzyme activity of proximal tubule cells occurring late in infection. It is suggested that the two lesions could have a different aetiology. The glomerular changes result from deposition of soluble trypanosome immune complexes, whereas the tubular changes are typical of tissue ischemia. Trypanosomiasis in the rabbit could be a valuable model for studies of the pathogenesis of renal damage in Rhodesiense sleeping sickness.
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