Renal disease in acute Plasmodium falciparum infection in man

Falciparum malaria is a complex disease with a broad clinical spectrum. Several pathophysiologic changes are involved in the disease process. Yet, in the complicated chain of events, these pathophysiologic phenomena are not specific and may be found in other acute inflammatory diseases. One of the most important effects of Plasmodium falciparum infection is capillary endothelial damage, which causes increased vascular permeability leading to an impairment in the microcirculation. Hemodynamic alteration, hematologic change, and immunologic response are among the major pathophysiologic mechanisms in the pathogenesis of the disease. Based on these mechanisms, renal involvement in falciparum malaria therefore varies widely. Disturbances in the renal microcirculation are responsible for acute renal failure; massive intravascular hemolysis causes hemoglobinuria with or without renal failure; and immunologic reaction to parasites accounts for glomerular lesions. In addition, fluid and electrolyte disorders may result from the nonspecific effect of fever. In this paper, the clinical spectrum of renal manifestations, renal pathologic changes, and pathogenesis will be presented