Severe Malaria and Associated Renal Dysfunction

Severe malaria, most often caused by Plasmodium falciparum, remains a critical public-health challenge in tropical regions, with multifaceted organ involvement including acute kidney injury (AKI). Renal dysfunction arises from a combination of factors: microvascular obstruction by parasitised erythrocytes, intravascular haemolysis releasing cell-free haemoglobin, oxidative stress and hypovolaemia. Clinical hallmarks include oliguria, rising serum creatinine and electrolyte imbalances. In paediatric cohorts, AKI complicates up to 40 % of severe malaria episodes and greatly increases both in-hospital and post-discharge mortality and long-term risk of chronic kidney disease (CKD). Pathogenic crosstalk between the kidney and distant organs—particularly the brain—has been proposed, whereby renal injury exacerbates blood–brain barrier disruption and contributes to neurocognitive impairment. Early recognition of renal involvement, point-of-care biomarkers and timely initiation of renal replacement therapy are pivotal to improving outcomes. Ongoing research seeks to refine risk stratification, elucidate molecular pathways of tubular injury and evaluate adjunctive therapies aimed at mitigating haemoglobin-mediated oxidative damage.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Severe Malaria and Associated Renal Dysfunction publication trend

The graph below shows the total number of articles in severe malaria and associated renal dysfunction across all publications each year (not limited to Nature Index journals).

Technical terms

Acute kidney injury (AKI): Sudden decline in renal function marked by elevated creatinine and reduced urine output, often reversible if promptly managed.

Chronic kidney disease (CKD): Progressive loss of kidney function over months or years, defined by persistent abnormalities in kidney structure or function.

Intravascular haemolysis: Destruction of red blood cells within circulation, releasing haemoglobin into plasma and triggering oxidative stress.

Oxidative stress: Cellular damage caused by reactive oxygen species, implicated in tubular epithelial injury in AKI.

Blood–brain barrier: Endothelial interface regulating passage of substances into the central nervous system; disruption contributes to cerebral complications.

References

1. The kidney–brain pathogenic axis in severe falciparum malaria. Trends in Parasitology (2023).
2. Acute kidney injury is associated with impaired cognition and chronic kidney disease in a prospective cohort of children with severe malaria. BMC Medicine (2019).
3. Cell-free hemoglobin mediated oxidative stress is associated with acute kidney injury and renal replacement therapy in severe falciparum malaria: an observational study. BMC Infectious Diseases (2017).