Abstract

AbstractDespite a great heterogeneity of clinical situations, the definition of acute kidney injury (AKI) is unique and its diagnosis includes an increase in serum creatinine and/or a decrease in diuresis. Contrary to the evolution of the biological markers of myocardial infarction observed for more than 50 years, it is always the “functional marker” creatinine which serves as the biological gold standard for the diagnosis of AKI. However, under the term of acute renal failure, very heterogeneous clinical situations are grouped together from an etiological, pathophysiological mechanisms, duration, evolution and associated complications. For fifteen/twenty years, new potential biomarkers have been studied and seem promising. Unlike troponin, which is increased in all types of myocardial infarction, these new biomarkers have different sensitivities and specificities depending on the type of AKI, which possibly explains their under-use in current practice.

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