Akutes Nierenversagen: Pathophysiologie und klinisches Management

Summary

The main pathomechanism of acute renal failure (ARF) is acute tubular necrosis (ATN) due to reduced perfusion of renal cortex resulting in ischemic injury. ATN has the potential for complete restitution. However, acute renal failure is often complicated by pre-existing renal disease, ongoing toxic injury or non-recovery of systemic circulation. From a clinical point of view, the reason of tubular injury may be based on pre-renal causes, glomerular- and/or interstitial disorders or obstructive nephropathy. Therapy must be specifically targeted on the underlying causes to overcome ARF. If kidney function is not reconstituted in an appropriate time period, renal replacement therapy has to be initiated. Recent evidence for improved patient survival supports an augmented dialysis dose to achieve a maximum of metabolic, volume and electrolyte control. To reach these goals, daily intermittend or continous forms of hemodialysis or hemofiltration are appropriate measures.

Schlüsselwörter

akutes Nierenversagen - Nierenersatztherapie - nephrotoxisch - Kontrastmittel-Nephropathie - intermittierende Hämodialyse - verlängerte Hämodialyse - tägliche Hämodialyse - SLEDD

Key words

acute renal failure, acute renal failure - renal replacement therapy - nephrotoxic - radiographic-contrast-agent-induced nephropathy - intermittend hemodialysis - prolonged hemodialysis - daily hemodialysis - SLEDD

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