Postconditioning is an effective strategy to reduce renal ischaemia/reperfusion injury

Background. Several recent studies have shown that a brief ischaemiaapplied during the onset of reperfusion (postconditioning) iscardioprotective in different animal models. The potential applicationof postconditioning to organs different from the heart, i.e.kidney, is not available and is investigated in the presentstudy. We also tested the hypothesis that mitochondria playa central role in renal protection during reperfusion. Methods. Wistar rats were subjected to left nephrectomy and90-min right kidney occlusion. In controls, the blood flow wasrestored without intervention. In postconditioned rats, completereperfusion was preceded by 3 min, 6 min and 12 min of reperfusionin a consecutive sequence, each separated by 5 min of reocclusion.Animals were studied for 48 h. Mitochondrial respiratory chainfunction, rate of hydroperoxide production and carbonyl proteinswere measured at the end of postconditioning and 24 h and 48h after reperfusion. Results. BUN and creatinine significantly decreased in the postconditioninggroup as compared to control rats. Mitochondrial respiratoryfunction was significantly impaired in control rats, mainlyat the level of Complex II. Postconditioning significantly reducedthis mitochondria impairment. The rate of mitochondrial peroxideproduction was higher in the control group than in the protectedgroup at the end of postconditioning reperfusion. Moreover,mitochondrial protein oxidation was significantly higher incontrol rats than in the postconditioning group at the end ofreperfusion. Conclusions. In the present study, postconditioning reducedrenal functional injury and reduces mitochondria respiratorychain impairment, mitochondria peroxide production and proteindamage.