Acute kidney injury (AKI) is a sudden decline in kidney function, often due to hemodynamic changes or a systemic nephrotoxic insult. Traditionally, kidney function has been measured by serum creatinine levels and urine output. However, in the setting of surgery, creatinine levels may not begin to rise until GFR has decreased by half, and urine output is usually decreased for various reasons. This has prompted the classification of AKI into the following types: 1) subclinical AKI, in which lab values and urine output do not meet the current classification systems and 2) functional AKI, in which lab values and urine output do meet the current classification systems.  The main classification systems used to define acute kidney injury are as follows: Acute Kidney Injury Network (AKIN); Risk, Injury, Failure, Loss, ESKD (RIFLE); and Kidney Disease Improving Global Outcomes (KDIGO). These criteria utilize serum creatinine (sCr) levels, glomerular filtration rate (GFR), and urine output. The criteria for each classification system are discussed below. AKIN classifies AKI if any of the following occurs within 48 hours: increased sCr x 1.5, sCr increase of 0.3 mg/dL or more, or urine output less than 0.5 mL/kg/h for over 6 hours. Some studies report that AKIN criteria are relatively less sensitive in capturing all episodes of AKI. RIFLE classifies AKI if any of the following occurs within 7 days: doubled sCr, decrease in GFR of more than 50%, or urine output less than 0.5 mL/kg/h. KDIGO classifies AKI if any of the following occurs: increase in sCr by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 hours; increase in sCr to 1.5 times baseline, which is presumed to have occurred within the prior 7 days; or urine volume less than 0.5 mL/kg/h for 6 hours. In terms of the time period of AKI versus acute kidney disease, the Acute Dialysis Quality Initiative Group states that acute kidney injury occurs within 48 hours or less, and acute kidney disease occurs when AKI lasts 7 or more days. The identification of AKI is now possible using several novel biomarkers, even at values that do not meet the conventional diagnostic criteria, a condition referred to as "subclinical AKI." Some of these markers represent structural damage to the kidney which may or may not affect its filtration capacity. Traditional criteria, such as plasma creatinine level, urine output, and less commonly cystatin C, measure the kidney's filtration ability rather than structural damage and, as such, can be labeled as "functional AKI." Although it might be tempting to dismiss AKI cases that don't align with traditional functional criteria as clinically insignificant, current evidence indicates that even a slight rise in perioperative creatinine levels is associated with a 50% rise in perioperative mortality and prolonged hospitalization. Perioperative acute kidney injury (AKI) is a serious yet underrecognized problem in patients who have recently undergone surgery. Due to increasing age and number of comorbidities, perioperative AKI is increasing in incidence and has significant associated morbidity and mortality. Postoperative AKI raises specific concerns as it elevates the risk of short- and long-term mortality, escalates hospitalization costs, and substantially increases resource utilization compared to patients without postoperative AKI. Early recognition of AKI and implementation of early goal-directed therapy is critical to reducing the incidence of progression to chronic kidney disease, renal replacement therapies (RRT), and death.