Recently, we have shown that remote ischemic preconditioning using the hind limb is effective in reducing renal ischemia/reperfusion injury (IRI). However, preconditioning is not applicable in patients suffering from an unpredictable ischemic insult. In contrast, ischemic postconditioning (IPostC) is a strategy to reduce injury after an ischemic insult, by inducing short-term ischemia/reperfusion (I/R) shortly after reperfusion of the target organ. Similarly, short-term I/R of a remote organ (RIPostC) may also confer protection to a target organ after IRI. We investigated whether IPostC and RIPostC induce protection after renal IRI, and whether these strategies have an additive effect. In anesthetized rats, we induced 25' ischemia in the right kidney and nephrectomised the left kidney. Subsequently, rats underwent no postconditioning, IPostC, RIPostC, or both. The local IPostC stimulus consisted of 6 cycles of 8"/8" I/R. The RIPostC stimulus consisted of 3 cycles of 4'/4' I/R of the hind limb. After 48h of reperfusion, an IRI-induced rise in plasma creatinine, plasma urea and fractional sodium excretion (FENa) was observed in the non-postconditioned control group. RIPostC alone reduced the FENa from 8.4±6.2% to 3.8±2.1%. Remarkably, the combination of IPostC + RIPostC caused a 45% reduction in plasma creatinine, from 288.4±124.3 to 152.6±38.8 mmol/l. Similarly, plasma urea was reduced from 38.4±11.1 to 22.3±7.1 mmol/l and FENa was reduced by >60% to 3.1±1.5% in the RIPostC + IPostC group. In conclusion, we found that RIPostC using the hind limb as remote organ can ameliorate renal function. Moreover, the combination of remote and local postconditioning is more powerful in reducing renal damage. Our observations suggest that IPostC and RIPostC may work via different mechanisms, leading to an additive effect of these strategies. This makes postconditioning a promising tool to prevent renal damage in e.g. renal transplantation.