Acute Kidney Injury in Non-falciparum Malaria

Abstract

Acute kidney injury (AKI) complicates non-falciparum malaria, particularly that from Plasmodium knowlesi. AKI (any KDIGO stage) is present in 20-30% of hospitalized patients with knowlesi malaria, with age >45 years having a sixfold risk of AKI. WHO-defined severe AKI (creatinine >265μmol/L) is found in ∼2.5% of adult knowlesi hospitalizations and 60% of deaths, with pathogenesis linked with intravascular hemolysis, endothelial activation, glycocalyx degradation and acute tubular necrosis (ATN). Paracetamol may have a renoprotective effect in severe knowlesi AKI, including reductions in medium-term proteinuria. WHO-severe AKI has been estimated by meta-analysis as occurring in 0.01% of combined hospital inpatient and outpatients with P. vivax malaria with unexplained geographic heterogeneity and incomplete systematic exclusion of comorbidities. Despite a paucity of community-based P. vivax KDIGO-defined AKI studies, one such study identified AKI in 10% of adults and children with vivax malaria, almost all KDIGO stage 1. AKI pathogenesis in vivax malaria is not well characterized; an exception is 8-aminoquinoline drug-induced acute hemolysis and ATN in patients with G6PD deficiency. AKI risk in malaria from P. malariae and P. ovale is poorly characterized and may be underrecognized. Long-term outcomes of AKI, including CKD and cardiovascular disease, are unknown in non-falciparum species, and longitudinal studies are needed.

Keywords: Plasmodium knowlesi; Plasmodium malariae; Plasmodium ovale; Plasmodium vivax; acute kidney injury; chronic kidney disease.