Renal failure in malaria: a pathophysiologic study.
A pathophysiologic study was made in 15 patients with acute renal failure due to falciparum malaria. Marked increase in plasma fibrinogen and elevation of serum fibrin degradation products were observed in all cases. The other coagulation parameters including prothrombin time, partial thromboplastin time, factor V and factor VIII were within the normal limits. Plasma hemoglobin was minimal. The blood viscosity was significantly increased. Blood volume study in 5 patients showed initial hypovolemia followed by hypervolemia and normovolemia. Decreased cortical renal blood flow was noted in renal hemodynamic study using 133Xe. Plasma renin activity was increased. Intravenous pyelography during the oliguric phase of renal failure revealed a poor nephrogram which increased in density at 24 and 48 h after the injection of the contrast material. The findings suggest the significance of reduction of renal blood flow in the pathogenesis of renal failure in human malaria. The roles of blood hyperviscosity and hypovolemia are emphasized.
D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology*; D000328:Adult; D001663:Bilirubin / Q000097:blood; D001806:Blood Urea Nitrogen; D001809:Blood Viscosity; D001810:Blood Volume; D003404:Creatinine / Q000097:blood; D005260:Female; D006400:Hematocrit; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000098:blood supply; D008288:Malaria / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow; D012083:Renin / Q000097:blood
D006454:Hemoglobins; D003404:Creatinine; D012083:Renin; D001663:Bilirubin