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Blood urea nitrogen (BUN) and serum creatinine (SCr) are not very sensitive and specific markers of kidney function in acute kidney injury (AKI) as they are influenced by many renal and nonrenal factors independent of kidney function. A biomarker that is released into the blood or urine by the injured kidney and is analogous to the troponin release by injured myocardial cells after myocardial ischemia or infarction, may be a more sensitive and specific early marker of AKI than BUN and SCr. Numerous biomarkers of AKI have been detected in the urine or serum of patients with AKI. Urine IL-18, urine NGAL, urine KIM-1, and urine L-FABP are biomarkers of renal tubular injury in early AKI and identify patients with AKI before the rise in BUN or SCr. Urine IL-18, urine NGAL, and urine KIM-1 are biomarkers of poor prognosis in patients with AKI. A combination of urinary TIMP2 and IGFBP7, which is known as NephroCheck is the first FDA-approved biomarker of AKI. Urinary [TIMP2] × [IGFBP7] of greater than 0.3 is an early biomarker of AKI and predicts outcomes. In the future, the combined use of functional and damage markers may advance the field of biomarkers of AKI. More studies are required to definitively demonstrate the association between early kidney damage biomarkers and clinical outcomes and to determine whether randomization to a treatment for AKI based on high structural/damage biomarker levels results in an improvement in kidney function and improves clinical outcomes.