Immunopathology of Acute Kidney Injury in Severe Malaria
Orestis Katsoulis1, Athina Georgiadou1,2, Aubrey J Cunnington1,2
1Section of Paediatric Infectious Disease, Department of Infectious Disease, Imperial College London, London, United Kingdom.
Abstract:
Acute kidney injury (AKI) is a common feature of severe malaria, and an independent risk factor for death. Previous research has suggested that an overactivation of the host inflammatory response is at least partly involved in mediating the kidney damage observed in P. falciparum patients with AKI, however the exact pathophysiology of AKI in severe malaria remains unknown. The purpose of this mini-review is to describe how different aspects of malaria pathology, including parasite sequestration, microvascular obstruction and extensive intravascular hemolysis, may interact with each other and contribute to the development of AKI in severe malaria, by amplifying the damaging effects of the host inflammatory response. Here, we highlight the importance of considering how the systemic effects and multi-organ involvement of malaria are intertwined with the localized effects on the kidney.
Insights
Severe malaria can cause acute kidney injury (AKI) through complex interactions. Understanding how parasite sequestration, hemolysis, and inflammation contribute to AKI is crucial for patient outcomes.
Area of Science:
- Malariology
- Nephrology
- Immunology
Background:
- Acute kidney injury (AKI) is a significant complication and mortality predictor in severe malaria.
- The precise mechanisms of AKI in severe malaria remain incompletely understood.
- Host inflammatory response overactivation is implicated, but its interaction with malaria pathology is unclear.
Purpose of the Study:
- To review the interplay of malaria pathologies in AKI development.
- To elucidate how parasite sequestration, microvascular obstruction, and hemolysis contribute to AKI.
- To emphasize the systemic and localized effects of malaria on kidney function.
Main Methods:
- Literature review and synthesis of existing research on severe malaria and AKI.
- Analysis of the pathophysiological mechanisms linking malaria and kidney damage.
- Discussion of the amplification of inflammatory responses by malaria-specific factors.
Main Results:
- Parasite sequestration, microvascular obstruction, and intravascular hemolysis are key contributors to AKI in severe malaria.
- These factors interact synergistically to amplify the host inflammatory response.
- Systemic malaria pathology significantly influences localized kidney damage.
Conclusions:
- AKI in severe malaria results from a complex interplay of parasitic, vascular, and inflammatory mechanisms.
- Understanding these interactions is vital for developing targeted therapies.
- Integrated approaches considering multi-organ involvement are necessary for managing severe malaria with AKI.
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Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury III: Clinical Manifestations
Acute Kidney Injury I: Introduction
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