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This study investigated the effects of malaria parasite infection on kidney function using albino Wistar rats. The aim of the study was to determine kidney impairment induced by malaria through controlled infection with Plasmodium berghei, a rodent malaria parasite closely similar to Plasmodium falciparum. Sixteen male Wistar rats (130–174 g) were divided into four groups:
control (uninfected), and three experimental groups infected with high (10⁶ iRBCs), medium (10⁴ iRBCs), and low (10² iRBCs) parasite doses, respectively. At the end of a 42-day experimental period, kidneys were harvested, processed, and examined histologically using hematoxylin and eosin staining. Results revealed dose-dependent renal pathology, with the high infection group showing a tendency of marked glomerular hypertrophy, tubular necrosis, vascular congestion, interstitial inflammatory infiltration, and hemosiderin casts, while moderate and mild changes were observed in the medium and low infection groups. Kidney weights however showed no significant increase in infected rats compared to controls, indicating parasitemia-related organomegaly. These findings demonstrate that malaria infection causes progressive, dose-dependent kidney damage characterized by glomerular and tubular injury, interstitial inflammation, and vascular alterations. In conclusion, malaria-associated nephropathy is a major complication of infection, and Plasmodium berghei-infected Wistar rats provide a reliable model for studying malaria-induced renal dysfunction and for evaluating potential
therapeutic interventions.
control (uninfected), and three experimental groups infected with high (10⁶ iRBCs), medium (10⁴ iRBCs), and low (10² iRBCs) parasite doses, respectively. At the end of a 42-day experimental period, kidneys were harvested, processed, and examined histologically using hematoxylin and eosin staining. Results revealed dose-dependent renal pathology, with the high infection group showing a tendency of marked glomerular hypertrophy, tubular necrosis, vascular congestion, interstitial inflammatory infiltration, and hemosiderin casts, while moderate and mild changes were observed in the medium and low infection groups. Kidney weights however showed no significant increase in infected rats compared to controls, indicating parasitemia-related organomegaly. These findings demonstrate that malaria infection causes progressive, dose-dependent kidney damage characterized by glomerular and tubular injury, interstitial inflammation, and vascular alterations. In conclusion, malaria-associated nephropathy is a major complication of infection, and Plasmodium berghei-infected Wistar rats provide a reliable model for studying malaria-induced renal dysfunction and for evaluating potential
therapeutic interventions.
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