Perioperative acute kidney injury (AKI) is a frequent complication that affects outcomes well beyond the perioperative period. Its mechanisms remain incompletely understood, arising from the interplay of comorbidities, surgical stress, and hemodynamic alterations. Assessment continues to rely on serum creatinine and estimated glomerular filtration rate, yet these measures are insensitive to early injury and may create a misleading impression of preserved renal function. Renal functional reserve testing is physiologically sound but impractical in clinical practice. Renal injury often precedes measurable rises in creatinine or urine output, a state described as subclinical AKI. During this stage, preserved renal functional reserve may mask injury, resulting in compensated kidney injury. Biomarkers such as neutrophil gelatinase-associated lipocalin and tissue inhibitor of metalloproteinases 2 are under active investigation, and refining biomarker panels may enhance the prediction of both onset and severity. Recognition of additional subphenotypes, including hypoperfusive, inflammatory, nephrotoxic, and obstructive forms, provides a framework aligned with pathophysiology and supports targeted strategies. Cardiac surgery represents a high-risk, data-rich setting in which perioperative AKI can be studied systematically. Interventions such as goal-directed perfusion during cardiopulmonary bypass, amino acid infusion, remote ischemic preconditioning, and dexmedetomidine have been tested in this context, though benefits remain inconsistent. Future directions include patient-specific simulation models, biomarker integration with electronic health records, and applications of artificial intelligence and implementation science. This review synthesizes current concepts and highlights the need for continued innovation to improve perioperative renal outcomes.