Cyclosporin in renal protection through strength of plasma NGAL and cystatin EC NGAL of urinary and KIM-1: study in experimental model of ischemia in rats and reperfusion

Abstract

Renal ischemia as a consequence of acute arterial occlusion, shock and organ transplantation is a common cause of cell injury, bankruptcy, delayed graft function and rejection kidney. After an acute ischemic event kidney, early reperfusion remains as the most effective strategy of damage control that body. However, reperfusion has the potential to cause cell death similar to that observed in the heart. New protection strategies to be used at the time of reperfusion are required to mitigate the damage. Renal ischemia-reperfusion injury results in cell damage and restricts the availability and function of kidneys donated for transplantation. One area of growing concern is the possibility of making a body resistant to injury by a subsequent ischemic insult prior ie the maneuver preconditioning. However, the potential for the protection of ischemic preconditioning has not been established in clinical practice because it requires an effective intervention before the onset of ischemia, which is often difficult to predict in non-surgical situations. A more affordable approach is to intervene early reperfusion, which is now under the control of the surgeon. The potential use of post-conditioning organs other than the heart, or kidney, has not been investigated in detail. The biggest technical problem is to establish the algorithm of postconditioning. In studies of postconditioning it is well established that there is a critical range of ischemia and reperfusion and that "suitable window" is sometimes difficult to establish. The post-ischemic renal affects the pathophysiological mechanism of ischemia reperfusion primarily through three procedures, namely, attenuation of ROS as well as a faster neutralization through removers (scavengers); preventing the formation of pores Temporary mitochondrial permeability as well as channels activation of mitochondrial ATP-dependent potassium and, finally, by inhibiting the inflammatory cascade, reducing both serum concentration of tumor necrosis factor. Objective of the research is to evaluate the protective effects of ischemic postconditioning and the use of cyclosporine A in experimental ischemia-reperfusion in rats and specific: to quantify the effectiveness of both the postconditioning kidney as cyclosporine A on protection kidney in a stress situation of ischemia and reperfusion by plasma NGAL and blood of Cys C, the urinary NGAL and KIM-1 and histological analysis. The topic is relevant because it can establish which biomarkers of kidney injury can early detect damage to the body, so you can set protection measures. Will be included in the study 40 male Wistar rats, weighing greater than or equal to 300 g were divided into four groups of 10 animals: group S or 01 (Sham), group C and 02 (Control), CsA group and 03 (A Ciclçosporina ) and PoC group or 04 (post-conditioning). All animals will be performed laparotomy and right nephrectomy. We will study the following attributes: systolic (SBP), diastolic (SD) and mean (MAP), heart rate (HR), rectal temperature, plasma levels of NGAL, Cys C, Na, K, Cr and Ur; dosages urinary NGAL, Kim-1, Na, Cr and Ur and histological examination of the kidneys in M1, M2 and M3. (AU)