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Ischemic acute injury of the kidney is a major cause of morbidity in kidneys. It occurs when the kidney is procured for transplantation. Reperfusion that follows a successful transplantation also increases the injury and is characterized by early inflammation. The inflammation is allo-antigen independent. Components of the innate immune system which include cytokines, chemokine and TLR’s contribute to pathogenesis of the injury. Cell mediated responses to the acute injury include macrophages, neutrophils and lymphocytes apart from the innate immune cells. In this review, we will focus on ischemic acute kidney injury and the immune mediators that participate in its pathogenesis (Jung and Rabbi, 2009).
Acute renal injury is characterized by renal function deteriorating within days. This deterioration results in the inability of the kidney to dispose toxic products, nitrogenous in nature, and maintain the balance of fluid and electrolyte. In the last fifty years, several important studies of Ischemic acute injury and renal failure of the kidney; and the mechanisms that cause dysfunction in the kidney have been done.
The topic here will involve around the recent studies done on Ischemic injury on different types of organs and its effect on the whole. This will create a grand picture and lay the foundation of the research document
Involves how the kidney injury is characterized, its symptoms, and the various stages of the injury.
Involves how the inflammatory cells cause a detrimental effect.
Involves how the pro-inflammatory leukocytes cause a detrimental effect (Ysebaert et al., 2000).
How the regulatory T cells provide a counter balance to the inflammation-causing cells of the immune system (Burne et al., 2001).
Cytokines play a vital role in regulating and the effector functions and the development of immune cells (Furuichi et al., 2006)
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