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Acute kidney injury (AKI) is one of the most serious complications of severe  Plasmodium falciparum  malaria, but the exact pathogenic mechanisms of AKI in  P. falciparum  infection have not been clearly elucidated. We hypothesized that oxidative stress is a potential mediator of acute tubular necrosis in  P. falciparum -infected kidneys. Therefore, this study aimed to investigate the histopathological changes and markers of oxidative stress in kidney tissues from mice with experimental malaria. DBA/2 mice were divided into two groups: the mice in the malaria - infected group ( n  = 10) were intraperitoneally injected with 1 × 10 6  P. berghei  ANKA-infected red blood cells, and the mice in the control group ( n  = 10) were intraperitoneally injected with a single dose of 0.85% normal saline. Kidney sections were collected and used for histopathological examination and the investigation of 4-hydroxynonenal (4-HNE) and heme oxygenase-1 (HO-1) expression through immunohistochemistry staining. The histopathology study revealed that the  P. berghei -infected kidneys exhibited a greater area of tubular necrosis than those of the control group ( p  < 0.05). The positive staining scores for 4-HNE and HO-1 expression in tubular epithelial cells of the  P. berghei -infected group were significantly higher than those found for the control group ( p  < 0.05). In addition, significant positive correlations were found between the tubular necrosis score and the positive staining scores for 4-HNE and HO-1 in the kidneys from the  P. berghei -infected group. In conclusion, this finding demonstrates that increased expression of 4-HNE and HO-1 might be involved in the pathogenesis of acute tubular damage in the kidneys during malaria infection. Our results provide new insights into the pathogenesis of malaria-associated AKI and might provide guidelines for the future development of a therapeutic intervention for malaria.

Expression of 4-Hydroxynonenal (4-HNE) and Heme Oxygenase-1 (HO-1) in the Kidneys of Plasmodium berghei-Infected Mice