Effect of Calcineurin Inhibitor on Blood Glucose Level in Non-Diabetic Kidney Transplant Patients
Background Calcineurin inhibitor (CNI) is a class of immunosuppressant agent used in kidney transplant management, known to pose risk for new-onset diabetes after transplant (NODAT). Tacrolimus and cyclosporine cause NODAT through multiple mechanisms, such as decreasing insulin secretion, increasing insulin resistance, and a direct effect on the pancreatic beta cell. Method This is a retrospective study on patients receiving immunosuppressant agents for kidney transplant patients in Surabaya. The immunosuppressant agents studied were CNI (tacrolimus and cyclosporine) in combination with mycophenolate mofetil (MMF) or azathioprine (Aza) and steroid. The blood glucose measured were fasting blood glucose (FBD) and 2-hour postprandial blood glucose (2PPBG). Objective Aim of this study is to determine the effect of calcineurin inhibitor (CNI) on glucose regulation in the nondiabetic renal transplant patient. Result Fifty-six subjects were included in the study, divided into two groups. One group of 28 patients (50%) received tacrolimus-MMF-MP and the other group received cyclosporine-MMF-MP. A significant increase in fasting blood glucose (pre-intervention level 86 ± 6 mg/dl vs post-intervention level 109 ± 34 mg/dl with p = 0.01) and 2-hour postprandial blood glucose (pre-intervention level 117 ± 20 mg/dl vs post-intervention level 150 ± 43 mg/dl with p < 0.001) was found in the tacrolimus group. A significant increase was also found in the cyclosporine group, both in fasting blood glucose (pre-intervention value 85 ± 7 mg/dl vs post-intervention value 97 ± 22 mg/dl with p = 0.002) and 2-hour postprandial blood glucose (pre-intervention value 119 ± 18 mg/dl vs post-intervention value 148 ± 55 mg/dl with p = 0.001). Tacrolimus was found to have a relative risk of NODAT up to 1.2 fold compared to cyclosporine. Conclusion Tacrolimus poses 1.29 relative risk of NODAT compared to cyclosporine. However, both drugs significantly increase fasting blood glucose and 2-hour postprandial blood glucose in non-diabetic patients receiving kidney transplantation.
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