Acute kidney injury (AKI) is a serious complication after cardiac extracorporeal circulation (CPB), significantly increasing the length of stay and mortality of patients. The mechanisms of acute kidney injury include a series of changes such as stress response, inflammation, hemodynamic changes and apoptosis. At present, no single mechanistic study has been able to give a completely reasonable explanation for AKI after CPB. The incidence of AKI after CPB has been reported in the literature to be as high as 1-30%, with a morbidity and mortality rate of 24-70%; and approximately 1-5% of these patients who develop AKI require renal replacement therapy. Age, history of COPD, combined renal artery stenosis, diabetes mellitus, low LVEF, preoperative use of aortic balloon counterpulsation, differences in surgical approach, emergency surgery, time to aortic block, and elevated preoperative blood creatinine have been reported in most of the current studies as major risk factors for AKI after CPB. However, most of these literature reports focus on preoperative and intraoperative related factors; we should also pay more attention to the prevention and treatment measures of AKI during postoperative period in ICU, and the long-term prognosis of such patients. Current studies have shown that hemodynamic disturbances due to low cardiac output in the early postoperative period are the most important factor leading to AKI. Patients with persistent low cardiac output (CI>2.2) or mean arterial pressure <40 mmHg for more than 24 h have a 3-fold increased risk of AKI due to inadequate renal vascular perfusion caused by the administration of high-dose vasoactive drugs. Postoperative hypoxemia is also a risk factor for AKI after CPB. Low oxygenation index (PaO2/FiO2>220), leading to organ hypoxia, should be highly alert for the occurrence of AKI. rapid atrial fibrillation, high chest drainage, pericardial tamponade, mediastinal infection, secondary intubation, and tracheotomy that are not promptly corrected after surgery are also high-risk factors for AKI. In terms of treatment, the primary management of patients with acute renal failure who fail to recover after removal of the causative factors, intensive monitoring, and reasonable adjustment of organ function is still renal replacement therapy. There is also no universally accepted and proven definitive effective method to prevent AKI after CPB. AKI is a dynamic pathophysiologic process involving multiple factors. Its treatment requires adequate evaluation and different management for its hemodynamic, inflammatory response and structural and functional cellular damage.