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.