Neuroendocrine stress response: implications for cardiac surgery-associated acute kidney injury

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J. Mauricio Del Rio, Alina Nicoara, Madhav Swaminathan
Department of Anesthesiology, Division of Cardiothoracic Anesthesiology and Critical Care Medicine, Duke University Health System, Durham, NC, USA


Surgical stress causes biochemical and physiologic perturbations of every homeostatic axis. These alterations include volume/baroreceptor regulation, sympathetic activation, parasympathetic suppression, neuroendocrine activation, acute phase response protein synthesis and secretion, immune response modulation and long-term behavioral adaptation. The kidney is central to the stress response because of its main role in the maintenance of water, electrolyte balance and hence, intracellular and extracellular compartments, including the intravascular volume. Acute kidney injury after cardiac surgery occurs as a result of numerous factors including ischemia-reperfusion, inflammation, oxidative stress, neurohormonal activation, metabolic factors, and nephrotoxicity or pigment nephropathy. The neuroendocrine stress response has a central role in initiating renal injury during cardiac surgery through an increased release of argininevasopressin and activation of the sympathetic nervous system and the intrarenal and systemic reninangiotensin-
aldosterone system. The contribution of an exaggerated neuroendocrine stress response to cardiac surgery and cardiopulmonary bypass as key pathophysiologic mechanism for acute kidney injury after cardiac surgery represents an opportunity for scientific exploration.

Keywords: surgical stress, neuroendocrine, acute kidney injury, cardiac surgery

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