Falciparum malaria characteristically causes severe complications because it produces the highest parasitic density in the blood, 100,000 to 500,000/mm3 versus 8000 to 20,000 mrrr' for plasmodium vivax and ovale, Furthermore P. falciparum attacks red cells in all its stages and exhibits the ability of multiple invasion of a single erythrocyte. Recent studies have shown serious pathophysiological changes in many vital organs, including acute renal failure, during severe falciparum malaria (1, 2). On many occasions the outcome of these patients is fatal. The mechanism consists of an endotoxin-like substance being released from parasitized red cells at schizogony and triggering the release of mediators from macrophages. These mediators, which appear to cause much of the illness manifested in malaria, include lymphocyte activating factor (LAF), tumor necrosis factor (TNF), glucocorticoid antagonising factor (GAF) and prostanoids such as thromboxane A2 (TXA 2) (2). In India malarial acute renal failure is seen predominantly in rain prone coastal provinces. About 300 patients are reported every year. Investigations suggest massive intravascular hemolysis induced by one of the following mechanisms a) anti-malarial drug therapy in 6-GPD deficient patients or b) quinine hypersensitivity (black-water fever) (3). Hemodynamic alterations like hypovolemia, hyperviscocity, catecholamine effect capillary endothelial damage leading on to increased permeability and disseminated intravascular coagulation (4). Cholestatic jaundice with severe hyperbilirubinemia. In acute falciparum malaria such cholestasis is very uncommon even in the most endemic areas of India. We have seen nine such patients in a total of 43 patients of malarial acute renal failure at our institute in last 10 years. All of these 9 patients had severe renal failure, cholestatic jaundice, and P. falciparum in peripheral blood. Blood urea and serum creatinine were elevated between 52.2-117.1 mmol/L and 735.91329 jlmol/L. The International Journal of Artificial Organs / Vol. 15/ no. 3, 1992/ pp. 133-134
[1]
V. Sitprija,et al.
Urine Uric Acid and Urine Creatinine Ratio in Acute Renal Failure
,
1984
.
[2]
V. Sitprija,et al.
Renal disease in acute Plasmodium falciparum infection in man.
,
1979,
Kidney international.
[3]
P. Singhal,et al.
Acute renal failure due to intravascular hemolysis in the North Indian patients
,
1977,
The American journal of the medical sciences.
[4]
J. Haynes,et al.
Evidence for differences in erythrocyte surface receptors for the malarial parasites, Plasmodium falciparum and Plasmodium knowlesi
,
1977,
The Journal of experimental medicine.
[5]
M. Bailey.
Endotoxin, bile salts and renal function in obstructive jaundice
,
1976,
The British journal of surgery.
[6]
W. Suki,et al.
Nature of the urinary concentrating defect in the Gunn strain of rat.
,
1969,
The American journal of physiology.
[7]
J. Dawson,et al.
Further Study into Obstructive Jaundice and Ischaemic Renal Damage
,
1969,
British medical journal.
[8]
T. Aoyagi,et al.
The effect of bile acids and renal ischemia on renal function.
,
1968,
The Journal of laboratory and clinical medicine.
[9]
J. Dawson,et al.
The incidence of postoperative renal failure in obstructive jaundice
,
1965,
The British journal of surgery.