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©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
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, 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
Processing time: 319 Days and 12.3 Hours
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
Processing time: 319 Days and 12.3 Hours
Core Tip
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.