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Transient Acute Kidney Injury in the Postoperative Period: It Is Time to Pay Closer Attention

Transient Acute Kidney Injury in the Postoperative Period: It Is Time to Pay Closer Attention Many of us have had the unsettling experience of watching the serum creatinine level rise or the urine output dwindle following a complex vascular operation. As kidney function deteriorates, we steel ourselves for the inevitable need for dialysis. The second guessing begins. Was it the contrast? The brief intraoperative hypotension? Or, perhaps a nephrotoxic drug? As the creatinine level ebbs, we breathe a sigh of relief. However, a growing body of literature indicates that we are lulled by a false sense of security. As highlighted in the article by Huber et al,1 transient acute kidney injury (AKI) in the postoperative period has lasting, long-term, mortal consequences on the heart. On first pass, it seems counterintuitive that a brief period of AKI would have lasting effects, particularly in a patient with normal kidney function at baseline. One must not forget, however, that an extreme loss of renal function is required to develop AKI in such patients. Alarmingly, nearly half of the patients in the study by Huber and colleagues developed AKI, and even transient AKI was associated with a 31% increase in 10-year adjusted cardiovascular mortality. This begs the question: what are the potential links between transient postoperative AKI and long-term cardiovascular death? The answer may lie in the concept of organ cross talk, which refers to the mechanism whereby injury of one organ affects the function of distant organs. The ischemia-reperfusion associated with AKI leads to an initial insult of the renal tubule and renal vascular endothelium.2 This appears to trigger a proinflammatory cascade, with the release of cellular and soluble mediators that lead to remote cardiac injury by various mechanisms including neutrophil infiltration, maladaptive neurohumoral responses, and cardiac myocyte apoptosis.3 An imbalance in cardiac homeostasis ensues, with the potential for long-term myocardial dysfunction. The results of the study by Huber and colleagues should prompt a call to action in terms of earlier diagnosis, treatment, and prevention of postoperative AKI. Recently, urinary markers of cell cycle arrest have been validated for the early identification of AKI far in advance of clinical manifestations such as oliguria or azotemia.4 These novel biomarkers may furnish physicians with a narrow window to reverse or altogether avoid the development of AKI. Goal-directed intraoperative measures to maximize renal perfusion and the early use of renal replacement therapy may also have a role in prevention and treatment, respectively. Perhaps even more exciting is the application of preoperative therapeutic interventions such as remote ischemic preconditioning, which in a recent trial was associated with a significantly reduced rate of AKI following cardiac surgery.5 Regardless of the strategies used, it is readily apparent that it is time to start paying closer attention to postoperative AKI. Back to top Article Information Corresponding Author: Christian de Virgilio, MD, Division of Vascular Surgery, Harbor-UCLA Medical Center, 1000 W Carson St, PO Box 25, Torrance, CA 90509 (cdevirgilio@labiomed.org). Published Online: December 23, 2015. doi:10.1001/jamasurg.2015.4660. Conflict of Interest Disclosures: None reported. References 1. Huber M, Ozrazgat-Baslanti T, Thottakkara P, Scali S, Bihorac A, Hobson C. Cardiovascular-specific mortality and kidney disease in patients undergoing vascular surgery [published online December 23, 2015]. JAMA Surg. doi:10.1001/jamasurg.2015.4526.Google Scholar 2. Amann K, Wanner C, Ritz E. Cross-talk between the kidney and the cardiovascular system. J Am Soc Nephrol. 2006;17(8):2112-2119.PubMedGoogle ScholarCrossref 3. Li X, Hassoun HT, Santora R, Rabb H. Organ crosstalk: the role of the kidney. Curr Opin Crit Care. 2009;15(6):481-487.PubMedGoogle ScholarCrossref 4. Bihorac A, Chawla LS, Shaw AD, et al. Validation of cell-cycle arrest biomarkers for acute kidney injury using clinical adjudication. Am J Respir Crit Care Med. 2014;189(8):932-939.PubMedGoogle ScholarCrossref 5. Zarbock A, Schmidt C, Van Aken H, et al; RenalRIPC Investigators. Effect of remote ischemic preconditioning on kidney injury among high-risk patients undergoing cardiac surgery: a randomized clinical trial. JAMA. 2015;313(21):2133-2141.PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Surgery American Medical Association

Transient Acute Kidney Injury in the Postoperative Period: It Is Time to Pay Closer Attention

JAMA Surgery , Volume 151 (5) – May 1, 2016

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Publisher
American Medical Association
Copyright
Copyright © 2016 American Medical Association. All Rights Reserved.
ISSN
2168-6254
eISSN
2168-6262
DOI
10.1001/jamasurg.2015.4660
Publisher site
See Article on Publisher Site

Abstract

Many of us have had the unsettling experience of watching the serum creatinine level rise or the urine output dwindle following a complex vascular operation. As kidney function deteriorates, we steel ourselves for the inevitable need for dialysis. The second guessing begins. Was it the contrast? The brief intraoperative hypotension? Or, perhaps a nephrotoxic drug? As the creatinine level ebbs, we breathe a sigh of relief. However, a growing body of literature indicates that we are lulled by a false sense of security. As highlighted in the article by Huber et al,1 transient acute kidney injury (AKI) in the postoperative period has lasting, long-term, mortal consequences on the heart. On first pass, it seems counterintuitive that a brief period of AKI would have lasting effects, particularly in a patient with normal kidney function at baseline. One must not forget, however, that an extreme loss of renal function is required to develop AKI in such patients. Alarmingly, nearly half of the patients in the study by Huber and colleagues developed AKI, and even transient AKI was associated with a 31% increase in 10-year adjusted cardiovascular mortality. This begs the question: what are the potential links between transient postoperative AKI and long-term cardiovascular death? The answer may lie in the concept of organ cross talk, which refers to the mechanism whereby injury of one organ affects the function of distant organs. The ischemia-reperfusion associated with AKI leads to an initial insult of the renal tubule and renal vascular endothelium.2 This appears to trigger a proinflammatory cascade, with the release of cellular and soluble mediators that lead to remote cardiac injury by various mechanisms including neutrophil infiltration, maladaptive neurohumoral responses, and cardiac myocyte apoptosis.3 An imbalance in cardiac homeostasis ensues, with the potential for long-term myocardial dysfunction. The results of the study by Huber and colleagues should prompt a call to action in terms of earlier diagnosis, treatment, and prevention of postoperative AKI. Recently, urinary markers of cell cycle arrest have been validated for the early identification of AKI far in advance of clinical manifestations such as oliguria or azotemia.4 These novel biomarkers may furnish physicians with a narrow window to reverse or altogether avoid the development of AKI. Goal-directed intraoperative measures to maximize renal perfusion and the early use of renal replacement therapy may also have a role in prevention and treatment, respectively. Perhaps even more exciting is the application of preoperative therapeutic interventions such as remote ischemic preconditioning, which in a recent trial was associated with a significantly reduced rate of AKI following cardiac surgery.5 Regardless of the strategies used, it is readily apparent that it is time to start paying closer attention to postoperative AKI. Back to top Article Information Corresponding Author: Christian de Virgilio, MD, Division of Vascular Surgery, Harbor-UCLA Medical Center, 1000 W Carson St, PO Box 25, Torrance, CA 90509 (cdevirgilio@labiomed.org). Published Online: December 23, 2015. doi:10.1001/jamasurg.2015.4660. Conflict of Interest Disclosures: None reported. References 1. Huber M, Ozrazgat-Baslanti T, Thottakkara P, Scali S, Bihorac A, Hobson C. Cardiovascular-specific mortality and kidney disease in patients undergoing vascular surgery [published online December 23, 2015]. JAMA Surg. doi:10.1001/jamasurg.2015.4526.Google Scholar 2. Amann K, Wanner C, Ritz E. Cross-talk between the kidney and the cardiovascular system. J Am Soc Nephrol. 2006;17(8):2112-2119.PubMedGoogle ScholarCrossref 3. Li X, Hassoun HT, Santora R, Rabb H. Organ crosstalk: the role of the kidney. Curr Opin Crit Care. 2009;15(6):481-487.PubMedGoogle ScholarCrossref 4. Bihorac A, Chawla LS, Shaw AD, et al. Validation of cell-cycle arrest biomarkers for acute kidney injury using clinical adjudication. Am J Respir Crit Care Med. 2014;189(8):932-939.PubMedGoogle ScholarCrossref 5. Zarbock A, Schmidt C, Van Aken H, et al; RenalRIPC Investigators. Effect of remote ischemic preconditioning on kidney injury among high-risk patients undergoing cardiac surgery: a randomized clinical trial. JAMA. 2015;313(21):2133-2141.PubMedGoogle ScholarCrossref

Journal

JAMA SurgeryAmerican Medical Association

Published: May 1, 2016

Keywords: ischemic preconditioning,postoperative ischemia,postoperative complications,renal failure, acute,biological markers,postoperative care,postoperative period,preoperative care,reperfusion injury,urinalysis,vascular surgical procedures,renal trauma,postoperative renal failure,monitoring, renal function,serum creatinine level,cardiovascular death

References

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