Renal complications are frequent and clinically significant in the perioperative period, with acute kidney injury (AKI) representing the most common manifestation. Postoperative AKI arises from a multifactorial interplay of patient comorbidities, surgical stress, hemodynamic fluctuations, and anesthetic management. In addition to classic mechanisms such as hypovolemia, hypotension, and nephrotoxin exposure, several surgery-specific contributors play a critical role. These include embolization from aortic plaque manipulation, non-pulsatile flow and systemic inflammatory activation during cardiopulmonary bypass, ischemia–reperfusion injury from vascular cross-clamping, and reperfusion syndrome in liver transplantation. The development of AKI is associated with increased short- and long-term morbidity, progression to chronic kidney disease, and higher mortality. Prevention strategies such as hemodynamic optimization, balanced fluid therapy, and avoidance of nephrotoxins remain the cornerstone of management, while treatment is largely supportive, with renal replacement therapy reserved for severe or refractory cases. Understanding both general and surgery-specific mechanisms of AKI is crucial to risk stratification, early recognition, and mitigation of renal complications.