Abstract

Post-transplant hyperglycemia and new-onset diabetes mellitus after transplantation (NODAT) are common and important metabolic complications. Decreased insulin secretion and increased insulin resistance are important to the pathophysiologic mechanism behind NODAT. However, the progression of glucose intolerance diagnosed late after kidney transplantation remains clearly unknown. Enrolled in this study were 94 kidney transplant recipients and 134 kidney transplant donors, as the healthy controls, who were treated at our institution. The 75 g-oral glucose tolerance test (OGTT) was performed in the recipients, and the healthy controls received an OGTT before donor nephrectomy. We assessed the prevalence of glucose intolerance including impaired fasting glucose and/or impaired glucose tolerance, as well as insulin secretion and insulin resistance using the homeostasis model assessment, and compared the results between the two groups. Multivariate analysis after adjustment for age, gender, body mass index, estimated glomerular filtration rate, and systolic blood pressure showed that the prevalence of glucose intolerance, insulin resistance, insulin secretion, and 2 h plasma glucose levels were significantly higher in the kidney transplant recipients compared to the healthy controls. Elevation of insulin secretion in kidney transplant recipients may be compensatory for increase of insulin resistance. Impaired compensatory pancreas β cell function may lead to glucose intolerance and NODAT in the future.

Highlights

  • Post-transplant hyperglycemia and new-onset diabetes mellitus after transplantation (NODAT) are common and significant metabolic complications in kidney transplant recipients (KTRs) which can lead to increased mortality and cardiovascular morbidity [1,2,3]

  • The aim of this study was to compare glucose tolerance between KTRs and healthy subjects using the oral glucose tolerance test (OGTT), and we assessed the prevalence of glucose intolerance including impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) as well as insulin secretion and insulin resistance using the homeostasis model assessment (HOMA)

  • The elevation of insulin secretion may be compensatory for the increase of insulin resistance in the KTR group

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Summary

Introduction

Post-transplant hyperglycemia and new-onset diabetes mellitus after transplantation (NODAT) are common and significant metabolic complications in kidney transplant recipients (KTRs) which can lead to increased mortality and cardiovascular morbidity [1,2,3]. Previous reports have shown that impaired insulin secretion is a more dominant mechanism for the development of NODAT compared to type 2 DM [5]. The increased prevalence of cardiovascular events in transplant recipients is an issue that remains to be solved. Abnormal glucose homeostasis is considered to be one of the established risk factors for the development of cardiovascular events following kidney transplantation [7], but there have been few reports comparing glucose tolerance between KTRs and healthy subjects

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