Theses
Date of Award
2026
Document Type
Thesis
Degree Name
Master of Science (MS)
Department
Biological Sciences
First Advisor
Dr.Julio Gallego-Delgado
Second Advisor
Dr. Stephen Redenti
Third Advisor
Dr. Pratyusha Mandal
Abstract
Malaria-associated acute Kidney injury (MAKI) is a severe manifestation caused by the Plasmodium falciparum infection. Up until recently, research in this area was highly neglected, and the impact of this severe malaria complication was greatly underestimated. Recent studies show a prevalence of MAKI in up to 45-60% of children with severe malaria. However, the underlying mechanisms contributing to this specific complication remain largely unknown. One potential contributor to MAKI pathogenesis is the excessive release of free hemoglobin during the asexual replication cycle of the parasite. The accumulation of free hemoglobin and, in turn iron, can lead to oxidative stress within the kidneys, setting the stage for ferroptosis, a unique form of regulated cell death driven by iron-dependent lipid peroxidation, which results in renal tubular damage. In this study, we aim to investigate the role of ferroptosis in the development of MAKI. Our data show the accumulation of iron deposits in the proximal tubules of mice infected with Plasmodium berghei NK65, demonstrated by Prussian Blue staining. Moreover, we have also observed elevated levels of 4-hydroxynonenal (4-HNE), a well-established marker of lipid peroxidation, in the malaria infected groups. Also, we have observed increased levels in key ferroptotic players such as glutathione peroxidase-4 (GPX4) and Heme-oxygenase-1 (HO-1) within the experimental groups. These findings advance our understanding of MAKI pathophysiology and set up the framework for the development of future therapeutic strategies targeting this severe complication of malaria.
Recommended Citation
Roberts, Alexandra V., "Ferroptosis is Activated During Malaria-Associated Acute Kidney Injury (MAKI)" (2026). CUNY Academic Works.
https://academicworks.cuny.edu/le_etds/50
