Abstract
"Acute kidney injury" (AKI) describes any acute deterioration in kidney function but also only injury to the kidneys without a severe loss of function. It is a common and severe complication in patients on the intensive care unit with a significant impact on patient's mortality and morbidity. Since no specific pharmacological therapy exists, the early identification of patients at risk for AKI or with acute kidney damage is most important before renal function further deteriorates. A stage-based management of AKI comprises more general measures like discontinuation of nephrotoxic agent but most importantly early hemodynamic stabilization. Recent research has contradicted that AKI is renal ischemia caused by vasoconstriction with consecutive tubular necrosis. In septic AKI renal blood flow is even increased. Intrarenal vasodilation together with microcirculatory changes and redistribution of blood flow are leading to a drop in glomerular filtration by functional changes. Accordingly, it had to be learned that not vasodilators, but vasoconstrictors are beneficial in AKI. A mean arterial blood pressure target of > 65 mmHg is often recommended but exact targets are not known and patients with preexisting hypertension do even need a higher perfusion pressure. Also, the concept that fluid therapy is always beneficial for the kidney in shock states had to be revised. A volume restrictive therapy with balanced, chloride restricted crystalloids only, is important also in AKI. Exposure to contrast material is often associated with AKI but less common the direct cause of AKI, so if indicated, contrast material should not be withheld in patients at risk for AKI.
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