Biomarkers for AKI

Abstract

Acute kidney injury (AKI) represents an abrupt decrease in renal function that leads to accumulation of nitrogenous waste products such as blood urea nitrogen and creatinine. AKI refers to a complex disorder that comprises multiple causative factors (ischemic, nephrotoxic and septic components with overlapping pathofysiological mechanisms) and occurs in a variety of settings with numerous clinical manifestations that range from minimal elevation in serum creatinine (SCr) to anuric renal failure. In the critical care setting, AKI affects 5-25% of patients and accounts for an overall mortality rate of 50- 80%] Once established the treatment of AKI is largely supportive, unsatisfactory and associated with a poor prognosis. Furthermore, AKI is independently associated with an increased risk of death and with a prolonged length of stay. Even small changes in SCr can affect outcome in severely ill patients with multiple-organ dysfunction. Progressive insight in pathofysiological mechanisms of AKI has shown that tubule cell necrosis is rarely encountered in human acute renal failure, indeed the disparity between the severe impairment of renal function and the relatively subtle histological changes in AKI have been bothersome.