[Recipient kidney damage after leukocyte transfer from inbred mice with renal ischemia-reperfusion injury]

In a recent study, we were able to demonstrate a role for leukocyte transfer in the induction of liver damage in recipient mice after induction of IR [60 min of bilateral renal artery occlusion and 3 hrs reperfusion] injury in donors. The present study investigates the role of leukocyte transfer in the induction of kidney damage in recipient mice after induction of renal IR injury in donors. Mice were divided into two sham and renal IR groups. After anesthesia, leukocytes were isolated from blood and were transferred to the two recipient groups: the intact recipient mice received leukocytes from the sham donor group [Sham recipient] and the intact recipient mice that received leukocytes from IR donor group [IR recipient]. After 24 hrs, the recipient mice were anesthetized and blood samples and renal tissues were collected. Renal malondialdehyde [MDA] increased and glutathione and superoxide dismutase [SOD] decreased significantly in IR recipient group in comparison to sham recipient group. Although renal function tests, including BUN and plasma creatinine were significantly different between IR donor and sham donor groups, but they were not significantly different in two recipient groups. Renal tissues in IR donor group showed extensive damage compared to sham group, but in IR recipients' kidneys, they were different from IR donor tissues despite being different from their respective sham group. These findings are suggestive of implication of leukocytes in renal tissue damage and oxidative stress after renal IR injury

[Evaluation of protective effects of postconditioning on ischemia/reperfusion-induced acute kidney injury]

In recent years, the role of reactive oxygen species [ROS] in ischemia-reperfusion injury [IRI] is established and different methods including ischemic preconditioning and postconditioning [POC] are introduced to reduce the damage. One of the possible protective mechanisms of POC is a reduction in ROS formation. According to the significance and prevalence of renal IRI, in the present study, the protective effect of POC on the reduction of IR-induced renal injury was evaluated. After right nephrectomy, male Sprague-Dawley rats were randomly assigned into three groups [n= 6]. In IR group, with the use of bulldog clamp 45 min of left renal artery was induced followed by 24 hours of reperfusion. In sham group, all of the above surgical procedures were applied except that IR was not induced. In POC group, after induction of 45 min ischemia, 4 cycles of 10 seconds of intermittent ischemia and reperfusion were applied before restoring of blood to the kidney. At the end of the experiments, serum and renal tissue samples were collected for renal functional monitoring and oxidative stress evaluation. POC prevented the IR-induced increase in blood urea Nitrogen and serum creatinine and improved the kidney oxidative status demonstrated by a decrease in malondialdehyde level and an increase in superoxide dismutase. POC has a protective role on renal function by a reduction in IR-induced oxidative stress