recent data demonstrate that impaired insulin secretion rather than impaired insulin sensitivity might be the principal pathophysiological defect in KTRs (7,8). Hence, antidiabetic drugs that protect or even improve pancreatic beta cell function may be especially advantageous in NODAT treatment (9). While beta cell protection through early postoperative insulin administra- tion has been shown effective against posttransplant hyperglycemia, and is thereby promising for NODAT prevention (5,10), solid evidence for antihyperglycemic
American Journal of Transplantation 2014; 14: 115–123 Wiley Periodicals Inc.
C Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons
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treatment of overt NODAT in stable KTRs is still scarce. A recent randomized controlled trial has evaluated the impact of the oral antidiabetic agents vildagliptin and pioglitazone compared to placebo, but importantly, in KTRs with prediabetes. Both agents were found to be safe and potentially effective in their application (11).