Akutes Nierenversagen

Abstract

Previously often regarded as only simple organ dysfunction which can easily compensated by modern renal replacement therapies, acute kidney injury (AKI) has lately been recognized as systemic proinflammatory, pro-oxidative syndrome, which independently from the severity of the underlying disease, exerts a fundamental impact on the course of disease, the evolution of complications, and outcome. Patients do not only die with but also from AKI. The causes of this fundamental impact of AKI on the course of disease and prognosis are based on the fact that AKI not only results in the well-known effects on volume and electrolyte balance but affects all biological functions and organ systems. AKI augments any inflammatory reaction, which results in distant organ injury of nonrenal organs, such as the lung, the heart, or the liver. Immunocompetence is massively compromised in AKI patients, and infections represent the most important cause of death in this patient group. These negative effects of AKI are mediated by three interrelated mechanisms: by acute uremic intoxication per se, by activation of cellular elements and release of cytokines by the injured kidney (the kidney as the "offender"), and by side effects caused by the type and intensity of renal replacement therapy. Because of the profound impact of AKI on the course of disease on short- and long-term prognosis, early diagnosis and initiation of preventive measures is of outmost importance to avoid the evolution of AKI. If AKI had become manifest, renal replacement therapy has to be adapted - regarding the optimal treatment modality, the timing, and therapy dose - in such manner as to minimize the negative side effects of AKI on the organism. Unfortunately, even modern renal replacement therapies are not able to simulate the complex renal functions and to fully compensate for the negative impact of AKI.