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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.
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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.
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Increase in blood viscosity due to
dehydration and hyperparasitemia also results in renal hypoperfusion.
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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.
See
pathology
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.
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.
See Quartan Nephropathy
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