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Author Notes:

Correspondence: Laurence Busse, Medical Director MS ICU, Emory Saint Joseph’s Hospital, 5665 Peachtree Dunwoody Road, Atlanta, GA 30342, USA.Medical Director MS ICUEmory Saint Joseph’s Hospital5665 Peachtree Dunwoody RoadAtlantaGA 30342USA Laurence.w.busse@emory.edu

LWB reports having received consulting fees from La Jolla Pharmaceutical Company.

The other author declared no competing interests.

Subjects:

Keywords:

  • acute kidney injury
  • angiotensin II
  • inflammation
  • intravenous fluids
  • oxidative stress

Novel Therapies for Acute Kidney Injury

Tools:

Journal Title:

Kidney International Reports

Volume:

Volume 2, Number 5

Publisher:

, Pages 785-799

Type of Work:

Article | Final Publisher PDF

Abstract:

Acute kidney injury (AKI) is a common disease with a complex pathophysiology. The old paradigm of identifying renal injury based on location—prerenal, intrarenal, and postrenal—is now being supplanted with a new paradigm based on observable kidney injury patterns. The pathophysiology of AKI on a molecular and microanatomical level includes inflammation, immune dysregulation, oxidative injury, and impaired microcirculation. Treatment has traditionally been supportive, including the avoidance of nephrotoxins, judicious volume and blood pressure management, hemodynamic monitoring, and renal replacement therapy. Fluid overload and chloride-rich fluids are now implicated in the development of AKI, and resuscitation with a balanced, buffered solution at a conservative rate will mitigate risk. Novel therapies, which address specific observable kidney injury patterns include direct oxygen-free radical scavengers such as α-lipoic acid, curcumin, sodium-2-mercaptoethane sulphonate, propofol, and selenium. In addition, angiotensin II and adenosine receptor antagonists hope to ameliorate kidney injury via manipulation of renal hemodynamics and tubulo-glomerular feedback. Alkaline phosphatase, sphingosine 1 phosphate analogues, and dipeptidylpeptidase-4 inhibitors counteract kidney injury via manipulation of inflammatory pathways. Finally, genetic modifiers such as 5INP may mitigate AKI via transcriptive processes.

Copyright information:

© 2017 International Society of Nephrology. Published by Elsevier Inc.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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