Renal disease in acute Plasmodium falciparum infection in man

Abstract

Renal failure in falciparum malaria is due to renal ischemia brought about by several pathophysiologic changes. The chain of events starts from the release, as an inflammatory response, of chemical substances which include histamine, denosine, kinins, and other vascular permeability factors. Capillary permeability is thus increased, allowing the escape of protein and water, which results in hypovolemia. Both kinins and hypovolemia stimulate catecholamine release, causing vasoconstriction. A combination of hypovolemia, catecholamine effect, and hyperviscosity along with plugging of parasitized erythrocytes during the late stage of the disease leads to impairment of renal microcirculation and renal failure. Finally, cytotoxic factor, detected in the blood late in the course of the disease, could further contribute to cellular damage.