Approximately 7% of patients undergoing non-cardiac surgery with general anesthesia develop postoperative acute kidney injury (AKI). It is well-known that general anesthesia may have an impact on renal function and water balance regulation, but the mechanisms and potential differences between anesthetics are not yet completely clear. Recently published large animal studies have demonstrated that volatile (gas) anesthesia stimulates the renal sympathetic nervous system more than intravenous propofol anesthesia, resulting in decreased water and sodium excretion and reduced renal perfusion and oxygenation. Whether this is the case also in humans remains to be clarified. Increased renal sympathetic nerve activity may impair renal excretory function and oxygenation and induce structural injury in ischemic AKI models and could therefore be a contributing factor to AKI in the perioperative setting. This review summarizes anesthetic agents' effects on the renal sympathetic nervous system that may be important in the pathogenesis of perioperative AKI.
Keywords: Acute kidney injury; anesthesia; propofol; renal sympathetic nerve activity; sevoflurane.
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