Abstract: Abstract: It has been well-documented that ICAM-1 is implicates in pathophysiology of ischemic-reperfusion injury in the kidney. Renal injury after ischemia appears to be a consequence of not only tissue hypoxia from interrupted blood supply but also from the process of reperfusion which leads to an active inflammatory process. Infiltrating leukocytes are the potential source of reactive oxygen species. Proteolytic enzymes and cytokines, which during reperfusion may play a detrimental role. It has been suggested that ICAM-1 plays a key role during leukocyte adhesion and recruitment to inflamed tissue. The goal of the review is to explore the effect and significance of ICAM-1 as well as its mechanism in renal ischemia-reperfunsion.