الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Acute kidney injury (AKI) is a common clinical event that disrupts kidney homeostasis, leading to unacceptably high morbidity and mortality.Renal ischemia/reperfusion injury (RIRI) remainsthe major cause of AKI that is observed ina variety of clinical situations such as renal transplantation and cardiovascular anesthesia.
In ischemic acute kidney injury, hypoxic and anoxic cell injuries occur early during the ischemic phase, followed by inflammatory responses in the reperfusion phase. During reperfusion, blood containing innate immune component flows through ischemic tissues and accentuates injury.Recent evidence has shown that immune phenomena are clearly related to the IRI, which initially activates an innate immune response followed by adaptive immune responses. Based on these observations, it was hypothesized that immunosuppressive drugs may prevent IRI.
During an acute inflammatory state, stimuli cause monocytes to release cytokines as TNF-α which upregulates the formation of chemokines as MCP-1 which is a potent chemokine that facilitates the recruitment of neutrophils and macrophages to inflammatory sites, which in turn, release reactive oxygen species (ROS) and myeloperoxidase (MPO). Oxidative stress occurs when a balance is disrupted by excessive production of ROS and/or by inadequate antioxidant defenses, including SOD and reduced GSH. ROS can also enhance lipid peroxidation of mitochondrial and plasma membranes which is indicated by increased levels of malondialdhyde (MDA).