[Acute Kidney Injury: Epidemiology, Pathophysiology, Repair Mechanisms].

Acute kidney injury (AKI) is a major complication in critically ill patients and affects up to 50% of those admitted to intensive care units. Causes of AKI include patient specific factors (susceptibility: e.g. age, pre-existing chronic kidney disease, chronic heart failure, diabetes) and patient unspecific factors (exposure: e.g. sepsis, hypovolemia, cardiac surgery, nephrotoxin application). Mortality of severe AKI is in the range of 40 - 50%.AKI is accompanied by volume overload, electrolyte disorders, acidosis, and uremia. The diagnosis of AKI is based on an increase of creatinine levels and/or a decrease in urine output within 7 days after an insult. These 2 markers are late und unspecific, especially with regard to early identification of patients at risk of AKI. New AKI markers have been investigated within the last decade including NGAL (neutrophil gelatinase-associated lipocalin), the product of IGFBP-7 (insulin like growth factor binding protein 7) and TIMP-2 (tissue inhibitor of metalloproteinase 2), KIM-1 (kidney injury molecule 1) and the cysteine-protease-inhibitor cystatin C. New markers or a panel of new markers might improve the diagnosis of patients at risk of AKI in the future.There are currently no specific therapeutics in the treatment of AKI. Therefore, the prevention of AKI is of an utmost importance. The recommended preventive measures include optimization of hemodynamics and volume status, close monitoring of creatinine levels and urine output, avoidance or discontinuation of nephrotoxic drugs, normoglycemia and the application of alternatives to radiocontrast agents if possible.As the long term prognosis of AKI highly depends on renal recovery, the 2 major goals for the future will be 1) the early identification of patients at AKI risk and 2) the support of renal recovery of AKI patients.