RESUMO
Incidence of acute kidney injury (AKI) is increasing and despite advances in supportive care, mortality from AKI in critically ill patients still exceeds 50%. Major causes of AKI can be classified into prerenal, renal and postrenal AKI and many of prerenal or ischemic acute tubular necrosis (ATN) are caused by decreased renal blood flow. In addition, exposure to nephrotoxicant or diverse drugs can lead to AKI and diseases that affect larger renal vessels, glomeruli, or renal microvasculature are also other causes of AKI. Because type of renal injury or initiation of proper therapy in setting of AKI is important in determining patient prognosis, differential diagnosis utilizing patients history, physical examination, and laboratory data including urinalysis, urine diagnostic indices, radiologic examination is important. Lack of sensitive biomarkers for early detection of AKI, which resembles troponin in acute myocardial infarction is one critical factor that has hampered the successful translation of various therapeutic strategies that were effective in animal research. However, over the last decade, efforts to identify and validate novel urine or plasma biomarkers in AKI led to identification of several promising biomarkers including neutrophil gelatinase associated lipocalin (NGAL), interleukin-18 (IL-18), cystatin-C and liver type fatty acid binding protein (L-FABP). Although far from replacing serum creatinine in clinical practice yet, data from large clinical studies are promising and here I briefly reviewed the characteristics of them and possible clinical utility in AKI.