Renal failure in malaria

Abstract

Acute renal failure (ARF) is seen mostly in Plasmodium falciparum infection, but P vivax and P. malariae can occasionally contribute for renal impairment. Malarial ARF is commonly found in non-immune adults and older children with falciparum malaria. Occurance of ARF in severe falciparum malaria is quite common in southeast Asia and Indian subcontinent where intensity of malaria transmission is usually low with occasional microfoci of intense transmission. Since precise mechanism of malarial ARF is not known, several hypotheses including mechanical obstruction by infected erythrocytes, immune mediated glomerular and tubular pathology, fluid loss due to multiple mechanisms and alterations in the renal microcirculation, etc, have been proposed. Increased fluid administration, oxygen toxicity, and yet unidentified factors may contribute to pulmonary edema, acute respiratory distress syndrome (ARDS), multiorgan failure and death. Mainstay of treatment consists of appropriate antimalarial drug therapy, fluid replacement, and renal replacement therapy. Loop diuretics can convert an oliguric renal failure to non-oliguric renal failure without affecting outcome of the disease though the conversion reduces the risk of volume overload. There is little evidence on beneficial effect of vasoactive drugs. Nephrotoxic drugs such as ACE inhibitors, NSAIDs, aminoglycosides, cephalosporins should be avoided. Currently, high quality intensive care, early institution of renal replacement therapy, and avoidance of nephrotoxic drugs are standard practice of the prevention and management of ARF.