Cellular damage after reperfusion of ischaemic tissue is defined as ischaemia-reperfusion injury (IRI). Hypothermia is able to decrease oxygen consumption, preventing a rapid loss of mitochondrial activity. However, even though cooling can help to decrease the deleterious effects of ischaemia, the consequences are not exclusively beneficial, such that hypothermic storage is a compromise between benefits and harm. The present review details the relationship between renal IRI and hypothermia, describing the pathophysiology of IRI and hypothermic protection through experimental evidence. Although experimental models of renal IRI are a valuable tool for understanding the pathophysiology of renal ischaemia-reperfusion, the clinical transfer of experimental results has several limitations, particularly because of anatomical and physiological differences. In this review limitations of animal models but also hypothermia as a strategy to protect the kidney from IRI are discussed. We also attempt to describe three clinical scenarios where hypothermia is used in clinical settings of IRI: transplantation, deceased donors and post-cardiac arrest.