It can be suggested that
pathophysiology of malaria infection was usually associated
with an activation of immune system and comprehends a
complex network with production of ROS, oxidative stress,
and inflammation [24–28]. It has also been described that
the erythrocyte destruction during blood stage of infection
accumulated high levels of toxic free heme in circulation that
had the ability to induce oxidative stress from production
of hydroxyl radicals via the Fenton/Haber-Weiss reaction
and resulting renal injury [29–31]. Apoptosis of renal tissues
during malaria infection has also been suggested in renal
injury [30]. Additionally, pathogenesis of malaria-associated
renal injury is most likely to be due to immune-complexmediated
glomerulonephritis caused by immune-complex
deposition and endothelial damage, which may lead to fatal
forms of malarial nephropathies