Abstract

Background: New-onset diabetes after transplantation has a significant negative impact on allograft and patient survival, and glucose intolerance (impaired fasting glucose; IFG and/or impaired glucose tolerance; IGT) is asymptomatic hyperglycemia and borderline diabetes. Previous reports have shown that glucose intolerance is a risk factor for diabetes and cardiovascular disease in general populations. However, the clinical significance of glucose intolerance in renal transplant recipients has not been identified. Measurements of the intimal-medial thickness (IMT) of the carotid arteries by B-mode ultrasound and pulse wave velocity (PWV) have been identified as non-invasive methods for assessing atherosclerosis. Our study was designed to determine whether glucose intolerance affects the occurrence of atherosclerosis by the evaluation of IMT and PWV in renal transplant recipients. Patients and methods: A total of 32 renal transplant recipients without prior evidence of diabetes (at least a year after transplantation) at our institution was enrolled in this study. Transplant recipients were divided into two groups (normal glucose tolerance (NGT) group and glucose intolerance group) according to the results of their oral glucose tolerance test with 75 g of glucose (OGTT). NGT was defined as fasting plasma glucose (FPG) < 110 mg/dl and 2h plasma glucose < 140 mg/dl, IFG as 110-126 mg/dl and < 140 mg/dl, IGT as < 110 mg/dl and 140-200 mg/dl, and diabetes mellitus (DM) as >126 mg/dl and >200 mg/dl, respectively. Glucose intolerance included IFG, IGT, IFG/IGT, and DM. Categories of glucose tolerance were defined according to the World Health Organization criteria. NGT was detected in 19 patients as assessed by OGTT, while 13 patients had glucose intolerance; 6 had IGT, 2 had IFG, and 5 had IGT and IFG. No patients had DM. Bilateral brachial-ankle PWV (baPWV) and IMT were measured as markers of atherosclerosis and compared between the subjects with glucose intolerance and those with NGT among the renal transplant recipients. Insulin resistance was estimated using the homeostasis model assessment of insulin resistance (HOMA-R), and pancreatic β-cell function was evaluated by the homeostasis model assessment of β-cell function (HOMA-β) and insulinogenic index. Results: The patients in the glucose intolerance group showed significantly greater baPWV and IMT than the patients in the NGT group. There was no significant difference in HOMA- β between the two groups, whereas insulinogenic index was significantly lower in the glucose intolerance group than in the NGT group. HOMA-R in the glucose intolerance group was significantly higher than that in the NGT group. Liner regression analysis showed that the rise in IMT in the renal transplant recipients significantly correlated with HOMA-R. Conclusions: This present study demonstrated that renal transplant recipients with glucose intolerance had increased IMT and baPWV. Our results suggested that glucose intolerance in renal transplant recipients may induce atherosclerosis, and that the rise in insulin resistance may contribute to the increased IMT in renal transplant recipients.

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