Abstract: SA-PO0044
Ague and AKI: Mosquitoes or Motrin
Session Information
- AKI: Novel Patient Populations and Case Reports
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Silverberg, Rachael A., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Malone, Laura, Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Joshi, Megha Raj, Walter Reed National Military Medical Center, Bethesda, Maryland, United States
- Kim, Myungjin G., Walter Reed National Military Medical Center, Bethesda, Maryland, United States
Introduction
Acute renal failure (ARF) is a known complication of severe malaria with proposed mechanisms of parasite sequestration, systemic inflammation, endothelial dysfunction, intravascular hemolysis, and hemodynamic compromise. Various histopathological lesions have been reported, including acute tubular necrosis, interstitial nephritis, and glomerulonephritis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are more frequently implicated in ARF with similar potential for varied patterns of injury. This case highlights the importance of a thorough travel history even when more common risk factors exist.
Case Description
A 21-year-old male presented with fever, malaise, and vomiting for two weeks. He took ibuprofen three times daily. Lab studies revealed ARF with nephrotic-range proteinuria with evidence of hemolysis. Vasopressor support was initiated for shock unresponsive to fluid resuscitation.
His urine sediment demonstrated renal tubular epithelial cells and rare granular casts. Imaging was notable for hepatosplenomegaly. Secondary work-up showed low C3. Blood and urine cultures, HIV, viral hepatitis, anti-GBM, dsDNA, ANCA, SPEP/UPEP and ADAMTS13 activity were unremarkable.
Renal biopsy noted extensive acute tubular injury and diffuse foot process effacement with interstitial fibrosis and tubular atrophy <5%. Immunofluorescence had non-specific background staining; no immune complex deposition was seen on electron microscopy.
Despite initial denial of travel, persistent inflammatory symptoms prompted further inquiry. The patient eventually disclosed recent trip to Nigeria with incomplete prophylaxis. Blood smear confirmed Plasmodium falciparum. He received IV artesunate therapy for severe malaria. Renal function and hemodynamics improved significantly, with recovery to baseline renal function and residual proteinuria <0.5 g/g.
Discussion
This case illustrates the diagnostic complexity of malaria-induced ARF, particularly in the context of coexisting nephrotoxic exposures as NSAIDs. P. falciparum can cause renal injury through immune activation, hemolysis, and circulatory compromise. A detailed travel history remains critical in evaluating patients with systemic symptoms and ARF, especially when alternate explanations as drug toxicity may obscure the diagnosis.
The views expressed above are those of the authors and do not reflect the official policy of the Army, Department of Defense, or US Government.