International Journal of Preventive Medicine · Published 2026-02-01 · DOI 10.4103/ijpvm.ijpvm_27_24
Pathogenesis of post-transplant diabetes mellitus (PTDM) in renal transplantation is not well established, but both IR and insulin deficiency are necessary for the appearance of PTDM. β-cell dysfunction is not the only player in the pathogenesis of diabetes; insulin resistance (IR) is also a risk factor for the development of T2DM in the general population. Generally, IR is highly prevalent in renal transplant recipients. Calcineurin inhibitors are still the mainstay of immunosuppression and can decrease insulin release from pancreatic β-cells. Changing tacrolimus to Cyclosporine to improve glucose metabolism in stable renal transplant recipients has been suggested in much of the previous literature. In studies comparing the efficacy of tacrolimus and Ciclosporin in preventing acute rejection and graft loss, tacrolimus has always been superior. However, the majority of studies comparing the two drugs reported higher incidents of PTDM with tacrolimus than Ciclosporin.
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