EHIZOGIE EGBEOBAUWAYE ADEYEMI

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.

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.

Malaria remains a significant global health challenge, with the spleen playing a crucial role in both parasite clearance and disease pathogenesis. This study investigated the histopathological effects of malaria parasites on the spleen using albino Wistar rats infected with varying concentrations of Plasmodium berghei. Sixteen rats were randomly divided into four groups: control (n=4), low infection (10² parasitized red blood cells, n=4), medium infection (10⁴ parasitized red blood cells, n=4), and high infection (10⁶ parasitized red blood cells, n=4). Animals were observed for 14 days before sacrifice and histopathological examination.All infected groups experienced significant weight loss compared to controls, with the high infection group showing the greatest reduction (-25.5±2.5g vs +17.0±0.0g in controls, p<0.001). The most striking finding was the paradoxical relationship between infection dose and spleen enlargement. The low infection group demonstrated the most pronounced splenomegaly (1.4±0.1g vs 0.7±0.1g in controls), representing a 100% increase in spleen weight. The splenic-somatic index confirmed this pattern, with the low infection group showing a two-fold increase (0.91% vs. 0.44% in controls, p<0.05). Surprisingly, histopathological examination revealed preserved tissue architecture across all groups, with normal white and red pulp organization despite significant organ enlargement. This suggests that early malaria-induced splenomegaly involvesprimarily functional rather than structural changes. The inverse dose-response relationship indicates that moderate infections may trigger optimal splenic activation, while severe infections may overwhelm the organ's adaptive capacity. These findings contribute to understanding malaria pathogenesis and emphasize that even low-level infections can have substantial physiological impacts, supporting the need for early intervention regardless of apparent infection severity.