Acute kidney injury (AKI) is a syndrome defined by acute increase of serum creatinine or decrease in glomerular filtration rate (GFR). AKI is common in patients undergoing cardiac surgery, imaging modalities and endovascular procedures with using iodinated contrast, those who suffer from sepsis and other critically ill patients. Serum creatinine, the current main diagnostic test for AKI, rises late in AKI pathophysiology and is not precise marker of acute changes in glomerular filtration rate. The serum creatinine measurements are confounded by a large number of variables, including age, gender, race, muscle mass, muscle metabolism, hydration status and medications. New studies presented laboratory markers of AKI detected in serum and urine. These include cystatin C, NGAL, KIM-1, L- FABP, IL-18 and others. These new biomarkers offer promise for early AKI diagnosis and for the depiction of severity of renal injury occurring with AKI. They can reflect the progression of AKI to chronic kidney disease (CKD). The aim of this article is to review specific biomarkers for early detection of AKI and progression to CKD.