The diagnosis of acute kidney injury (AKI) is routinely based on changes in serum creatinine, but its measurements are a poor indicator of acute deterioration in kidney function. First, serum creatinine concentrations might not change until about 50% of kidney function has already been lost. Second, serum creatinine levels can vary widely with age, sex, muscle mass, muscle metabolism, medications and hydration status. Novel, more specific and sensitive biomarkers of AKI are neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule 1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), which concentrations in both urine or serum rise significantly in patients with AKI and correlate with severity of kidney injury.