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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Aug 25, 2015; 6(10): 1132-1151
Published online Aug 25, 2015. doi: 10.4239/wjd.v6.i10.1132
Dysglycemia after renal transplantation: Definition, pathogenesis, outcomes and implications for management
David Langsford, Karen Dwyer
David Langsford, Karen Dwyer, Department of Nephrology, St Vincent’s Hospital Melbourne, Fitzroy 3065, Australia
Author contributions: Langsford D and Dwyer K contributed to this paper.
Conflict-of-interest statement: The authors declare that they have no competing interests.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Karen Dwyer, Department of Nephrology, St Vincent’s Hospital Melbourne, 59 Victoria Parade, Fitzroy 3065, Australia. karen.dwyer@svhm.org.au
Telephone: +61-3-92883112 Fax: +61-3-92313151
Received: October 11, 2014
Peer-review started: October 11, 2014
First decision: October 28, 2014
Revised: July 6, 2015
Accepted: August 16, 2015
Article in press: August 17, 2015
Published online: August 25, 2015
Abstract

New-onset diabetes after transplantation (NODAT) is major complication following renal transplantation. It commonly develops within 3-6 mo post-transplantation. The development of NODAT is associated with significant increase in risk of major cardiovascular events and cardiovascular death. Other dysglycemic states, such as impaired glucose tolerance are also associated with increasing risk of cardiovascular events. The pathogenesis of these dysglycemic states is complex. Older recipient age is a consistent major risk factor and the impact of calcineurin inhibitors and glucocorticoids has been well described. Glucocorticoids likely cause insulin resistance and calcineurin inhibitors likely cause β-cell toxicity. The impact of transplantation in incretin hormones remains to be clarified. The oral glucose tolerance test remains the best diagnostic test but other tests may be validated as screening tests. Possibly, NODAT can be prevented by administering insulin early in patients identified as high risk for NODAT. Once NODAT has been diagnosed altering immunosuppression may be acceptable, but creates the difficulty of balancing immunological with metabolic risk. With regard to hypoglycemic use, metformin may be the best option. Further research is needed to better understand the pathogenesis, identify high risk patients and to improve management options given the significant increased risk of major cardiovascular events and death.

Keywords: Management, Epidemiology, Pathogenesis, Renal transplantation, Diabetes

Core tip: New-onset diabetes after transplantation (NODAT) carries a significant cardiovascular burden. Its pathogenesis is multifactorial and includes modifiable factors. New insights into glucose and insulin homeostasis may lead to improved ability to identify high risk patients and to the development of management strategies that do not require alteration in immunosuppression, whilst simultaneously reducing the risk of NODAT.