Journal of Urology and Nephrology Open Access Open Access Short Communication are not consistent; some reported benefits [3-5], while others reported neutral effects [6,7]. Therefore, the aim of the present study is to develop an experimental RIPC model against Renal Ischemia/Reperfusion (I/R)-induced AKI for the further evaluation of complexity observed in the clinical studies. Methods and Materials Male C57BL/6 mice at 5 weeks of age were purchased from CLEA (Tokyo, Japan). The mice were uninephrectomized 10 days prior to I/R and RIPC. We examined seven different RIPC protocols to determine whether RIPC induces renal protection against renal I/R injury in either pentobarbital (Figure 1 and 2) or isoflurane (Figure 3) anesthetized mice. All experimental procedures were performed according to the guidelines for the care and use of animals established by Kagawa University. RIPC was conducted by occluding the femoral artery and vein in the right hind limb by noninvasive vascular clamp, except for one protocol using low temperature-induced ischemia. We observed the right hind limb turn white during ischemia, and return to normal color after reperfusion. Renal I/R were performed in the left kidney of animals that had received a right uninephrectomized 10 days prior to I/R, under body temperature-controlled condition. Blood Urea Nitrogen (BUN) level was assessed as previously described [2]. Plasma BUN levels were measured using commercially available assay kits (Urea nitrogen B test; Wako, Osaka, Japan). For the histology, kidney tissue was fixed with 4% par formaldehyde (pH = 7.4), embedding in paraffin and sectioned into 3 μm thick slides, and stained with hematoxylin/ eosin. We used an optical microscope (BX-51/DP-72; Olympus, Tokyo, Japan) to observe renal histological changes. Semi-quantitatively analyzed HE scores were given as average values of loss of the brush border, tubular dilatation, cast formation, and congestion/ hemorrhage.