Renal impairment is a sensitive prognostic indicator in severe falciparum malaria. Renal failure is more common in adults and rarely, if ever, seen in children. Usually there is a reversible dysfunction, which may progress to acute tubular necrosis and acute renal failure. It carries a high mortality.
Renal dysfunction in falciparum malaria can be due to many factors: Renal failure in malaria is caused by renal cortical vasoconstriction and resultant hypoperfusion, sequestration and resultant acute tubular necrosis due to microvascular obstruction and due to massive intravascular hemolysis in blackwater fever.
- Dehydration and hypovolumia can lead to renal hypoperfusion, but this is reversible with adequate rehydration. High-grade fever, profuse sweating, lack of adequate intake, vomiting and diarrhoea contribute to dehydration.
- Increase in blood viscosity due to dehydration and hyperparasitemia also results in renal hypoperfusion.
- Intravascular hemolysis and clogging of the tubules by the products of hemolysis is another important cause for renal dysfunction. Severe falciparum malaria results in hemolysis of parasitized as well as non-parasitized red cells. Oxidant drugs like primaquine can also contribute to hemolysis in severe falciparum malaria, and particularly in patients with deficiency of Glucose 6-phosphate dehydrogenase enzyme. Although hemoglobin itself is not nephrotoxic, other products of hemolysis can cause acute tubular necrosis, particularly in the presence of dehydration and acidosis.
Renal failure in malaria usually manifests as oliguria with urine output less than 400 ml in 24 hours. However in some cases it may be non-oliguric or polyuric.
Investigations: Blood urea, creatinine, electrolytes, bicarbonate, and urine analysis including urine specific gravity should be done. If the patient is severely ill and anuric, ECG can be done to identify hyperkalemia (tall, pointed T waves; widening of QRS). Hyperventilation with a clear chest indicates metabolic acidosis and in such cases, arterial pH and blood gases should also be estimated. All these parameters should be assessed twice every day in the initial stages of the disease.
Management:
See Treatment of Severe P. falciparum malaria
Provided that the patient has not been given diuretics, a specific gravity of more than 1.015 suggests dehydration and such patients may respond to rehydration. Normal saline should be infused until the central venous pressure rises to 5 cm of water. If this fails to improve the urine output, then Inj. Furoscemide can be given. Starting at 40 mg, the dose of furoscemide can be progressively increased at half-hourly intervals. Dopamine infusion at 2-5mg/kg/min can also be tried. If these measures fail to re-establish urine flow, further doses of these drugs as well as intravenous fluids should be withheld.
Dialysis should be considered in all patients who do not respond to this conservative treatment. Anuria after adequate fluid replacement, hyperkalemia, fluid overload, metabolic acidosis and clinical signs of uremia (pericarditis, encephalopathy) are indications for dialysis. The rate of exchange of dialysate should be governed by the improvement in biochemical parameters. High glucose dialysate (hypertonic) can be used to reduce fluid overload, which in addition takes care of hypoglycemia.
Hemodialysis is preferred over peritoneal dialysis for splanchnic blood flow may be reduced in severe malaria and solute clearance may be less across the peritoneum. However, if facilities are not available for hemodialysis, peritoneal dialysis can still be tried. It should be kept in mind that bleeding and secondary infections are high with this procedure in cases of severe malaria. Peritoneal dialysis should be carried out with Tenckhoff catheter inserted under aseptic precautions. Whenever there is suspicion of peritonitis, peritoneal effluent should be examined under Gram’s stain and it should be cultured. Appropriate antibiotics can be started based on the Gram’s stain report.
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