The duration of hyperthermic perfusion-rewarming temperature greater than 37°C-was an independent predictor of AKI. Avoidance of hyperthermic perfusion may be more beneficial in reducing AKI than avoidance of rewarming.

This review describes the risk factors related to cardiopulmonary bypass that contribute to the development of AKI, in particular the role of remote ischaemic preconditioning on the effect of pre-existing CKD. ABSTRACT:The incidence of acute kidney injury (AKI) is a frequent and serious complication of cardiac surgery. In 2013, 95% of cardiac surgical procedures performed in Australia and New Zealand used cardiopulmonary bypass (CPB). AKI following CPB is well known, yet the perioperative factors contributing to its development are incompletely understood. AKI following CPB has significant implications on both short-term and long-term outcomes. The techniques for conducting CPB have evolved, moving towards evidence-based practice; however, there is still no generally accepted definition of optimal perfusion and its conduct. This review examines the current incidence of AKI following cardiac surgery and the short-term and longer-term effects of AKI on morbidity and mortality. The purpose of this review is to discuss the perioperative risk factors related to CPB and their contribution to the development of AKI. This review will also discuss outcomes in regard to off-pump cardiac surgery, the role of remote ischaemic preconditioning on AKI and outcomes in patients with chronic renal failure undergoing cardiac surgery.

Brief periods of ischaemia followed by reperfusion of one tissue such as skeletal muscle can confer subsequent protection against ischaemia-induced injury in other organs such as the heart. Substantial evidence of this effect has been accrued in experimental animal models. However, the translation of this phenomenon to its use as a therapy in ischaemic disease has been largely disappointing without clear evidence of benefit in humans. Recently, innovative experimental observations have suggested that remote ischaemic preconditioning (RIPC) may be largely mediated through hypoxic inhibition of the oxygen-sensing enzyme PHD2, leading to enhanced levels of alpha-ketoglutarate and subsequent increases in circulating kynurenic acid (KYNA). These observations provide vital insights into the likely mechanisms of RIPC and a route to manipulating this mechanism towards therapeutic benefit by direct alteration of KYNA, alpha-ketoglutarate levels, PHD inhibition, or pharmacological targeting of the incompletely understood cardioprotective mechanism activated by KYNA.