Renal IRI, which is caused by cardiopulmonary bypass, partial nephrectomy, and renal transplantation, is an emerging clinical problem, because acute renal injury can result in end-stagerenal disease [32]. Chronic kidney disease increases the risk of death and cardiovascular morbidity, even when dialysis is unnecessary [33]. With this in mind, IPC may be an alternativestrategy to preserve renal function after IRI.In our previous study, we demonstrated that remote IPC with the late window group hadlower urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin(NGAL) levels than the control group following IRI [31]. Gardner et al. also demonstrated that remote IPC has a renoprotective effect in renal IRI in a porcine model [16]. Our results demonstrate that numerous gene expression levels were altered in the rIPC groups, especially in therIPCl group. Hanto et al. verified that intraoperative administration of inhaled carbon monoxide reduces delayed graft function in a porcine delayed kidney transplantation model [34]. Inthat study, the authors hypothesized that the expression of antioxidant, proinflammatory, andreparative gene families improved renal function. Jun et al. performed a microarray study demonstrating a protective effect for IPC in a lung IRI model [29]. In their study, the differentiallyexpressed genes had roles in inflammation, apoptosis, oxidation, antioxidation, and metabolism. While their study evaluated lung tissue rather than renal tissue, the microarray analysisresults are similar to those from our present study, which provides additional evidence for ourhypothesis that IPC affects numerous pathways rather than one specific pathway. Our microarray data suggest that IPC induces changes in the complement system, the coagulation cascade,and various cytokines and cytokine receptors.