Malarial nephropathy

Abstract

Malaria is widely prevalent in the tropics. Clinically significant renal and renal-related disorders commonly occur in infection with Plasmodium falciparum and P. malariae. Falciparum malaria causes fluid and electrolyte disorders, transient and mild glomerulonephritis, and acute renal failure (ARF). It appears that ARF is mediated by a complex interaction of mechanical, immunologic, cytokine, humoral, acute phase response, nonspecific factors, and hemodynamic factors. Parasitized erythrocytes play a central role in all aforementioned pathogenic factors of ARF. Antimalarial drugs are still the cornerstone of treatment of falciparum infection. Because of the hypercatabolic state of falciparum malaria-induced ARF, hemodialysis as well as peritoneal dialysis should be immediately performed when there is a rapid increase of creatinine concentration. P. malariae, in contradistinction, can cause chronic glomerulopathy that may relentlessly progress to end-stage renal disease. Antimalarial drugs, corticosteroids, and immunosuppressive agents are not effective.