Renal function impairment can be found in severe or complicated P. falciparum malaria. Some studies report 2-5% incidence of acute renal failure associated with high mortality (1). Causes of acute renal damage are not clearly understood but massive hemoglobinuria seems unlikely in the majority of cases and different immunopathogenic mechanisms leading to tubulointerstitial nephritis are currently proposed (2). Ultrastructure of renal lesions in malaria have been performed in humans (3) and in some infections of rodents and monkeys (4). These studies report abnormalities mainly in the glomerular area and references to tubular cell pathologic changes are still limited. This work describes tubular and capillary alterations in P. berghei malaria.

P. berghei parasitized erythrocytes (strain from the Swiss Tropical Medicine Institute) were inoculated intraperitoneally in C57BL/6 male mice. Renal samples were obtained at 13th-14th days post-infection when severe illness was evident and parasitaemia reached 40-50%. Samples were processed by routine techniques for transmission electron microscopy and observed in Hitachi H-500 and H-7100 electron microscopes.