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Acute Kidney Injury in Non-falciparum Malaria
Nicholas M Anstey1, Matthew J Grigg1, Timothy William2
1Global and Tropical Health Division, Menzies School of Health Research and Charles Darwin University, Darwin, Northern Territory, Australia; Infectious Diseases Society Sabah-Menzies School of Health Research Clinical Research Unit, Queen Elizabeth Hospital, Kota Kinabalu, Sabah, Malaysia.
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.
Insights
Acute kidney injury (AKI) is a significant complication of non-falciparum malaria, especially Plasmodium knowlesi. Risk factors include age, and pathogenesis involves hemolysis and tubular necrosis, necessitating further research into long-term outcomes.
Area of Science:
- Tropical Medicine
- Nephrology
- Infectious Diseases
Background:
- Acute kidney injury (AKI) is a known complication of malaria, particularly non-falciparum species.
- Plasmodium knowlesi malaria presents a significant risk for AKI, affecting 20-30% of hospitalized patients.
- Severe AKI is associated with high mortality in knowlesi malaria.
Purpose of the Study:
- To review the incidence, pathogenesis, and risk factors of AKI in non-falciparum malaria.
- To highlight the under-characterized AKI risk in Plasmodium vivax, Plasmodium malariae, and Plasmodium ovale infections.
- To emphasize the need for research on long-term outcomes of AKI in non-falciparum malaria.
Main Methods:
- Literature review and meta-analysis of existing studies on AKI in non-falciparum malaria.
- Analysis of KDIGO (Kidney Disease: Improving Global Outcomes) staging for AKI.
- Examination of pathogenetic mechanisms including intravascular hemolysis and acute tubular necrosis (ATN).
Main Results:
- Age over 45 is a sixfold risk factor for AKI in knowlesi malaria.
- Severe AKI occurs in ~2.5% of knowlesi malaria hospitalizations and is linked to mortality.
- AKI in P. vivax malaria is less severe but occurs in ~10% in community settings; pathogenesis is often linked to G6PD deficiency and 8-aminoquinoline drugs.
Conclusions:
- AKI is a critical concern in non-falciparum malaria, with P. knowlesi posing the highest risk.
- Pathogenesis involves hemolysis and ATN, with potential renoprotective effects of paracetamol noted.
- Long-term consequences of AKI in these infections remain largely unknown, requiring further investigation.
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