Acetaminophen as Renoprotective Treatment in a Patient With Severe Malaria
Background: Severe falciparum malaria with renal impairment carries a significant risk of poor outcomes, including death. Previous randomized controlled trials using acetaminophen as adjunctive treatment for malaria-associated renal failure have demonstrated improvements in renal function and kidney injury progression.
Case Presentation: A 50-year-old man with severe falciparum malaria presented with hemolytic anemia, oliguric acute kidney injury, nephrotic range proteinuria, and significant architectural changes on renal ultrasound. Treatment with oral acetaminophen 975 mg every 6 hours was based on the randomized controlled trial protocol to salvage his renal function and avoid dialysis. During the acetaminophen course, urine output and cystatin C level improved with only mild, asymptomatic elevations in aminotransferases that were corrected on follow-up. The patient recovered without requiring dialysis.
Conclusions: Acetaminophen’s potential to mitigate the oxidative damage of hemoproteins suggests its use as a treatment in severe malaria with renal impairment.
In this case of severe falciparum malaria, the patient demonstrated renal impairment with measured falciparum parasitemia. His creatinine level and BUN appeared to stabilize and improve after 72 hours of acetaminophen administration. A recovery of urine output and improvement in cystatin C occurred during the 72 hours of acetaminophen usage. Despite the patient’s underlying chronic kidney disease, measured proteinuria, and significant changes in renal architecture revealed by ultrasound, he never showed signs of uremia, fluid overload, electrolyte derangements, or acidosis requiring urgent renal replacement therapy.
The patient’s treatment for severe falciparum malaria, including a combination of supportive management, acetaminophen, and IV antimalarials, resulted in the resolution of parasitemia and symptoms with some recovery of renal function without necessitating renal replacement therapy. Maximum daily doses of acetaminophen compared with the control in the Plewes and colleagues acetaminophen trial resulted in moderate increases in aminotransferases not rising to the criteria of hepatotoxicity described in Hy’s law.5 Following acetaminophen administration, in this case, AST and ALT levels peaked at 130 and 168 IU/L, 2.8 and 3.8 times the upper limits of normal, respectively. These mild, asymptomatic elevations in aminotransferases recovered to within normal limits, measuring 24 and 13 IU/L at the follow-up.
Conclusions
The demonstrated recovery in renal function, with only a transient, moderate increase in aminotransferases, supports the value of adjunctive acetaminophen as a renoprotective treatment in severe malaria. This simple, readily available treatment may significantly alter the morbidity and mortality associated with severe malaria.
