Abstract:
Background: Advances in immunosuppressive therapy have significantly improved graft survival and
overall outcomes after solid organ transplantation. However, metabolic complications, particularly
new-onset diabetes after transplantation (NODAT), remain common and are associated with increased
cardiovascular risk, graft dysfunction, and mortality. Effective strategies for the prevention and
management of post-transplant hyperglycemia are therefore essential.
Methods: A narrative review of English-language publications indexed in the PubMed database during
the last 10 years was conducted to evaluate the mechanisms of immunosuppressant-induced
disturbances in glucose metabolism and to assess the potential role of metformin in the management
of post-transplant hyperglycemia.
Results: Pharmacological therapy combined with lifestyle modification represents a key approach for
glycemic control in transplant recipients. Metformin, widely used as first-line therapy in type 2
diabetes mellitus, has been increasingly considered for patients with NODAT. Through improvement
of insulin sensitivity and inhibition of hepatic gluconeogenesis, metformin may counteract
hyperglycemic effects induced by commonly used immunosuppressive agents, including calcineurin
inhibitors (cyclosporine, tacrolimus), mammalian target of rapamycin (mTOR) inhibitors (sirolimus,
everolimus), and glucocorticoids. Additionally, metformin may help limit weight gain associated with
chronic corticosteroid therapy.
Conclusions: Metformin represents a valuable therapeutic option for the management of posttransplant hyperglycemia and NODAT due to its favorable metabolic profile, low risk of
hypoglycemia, and limited interaction with immunosuppressive therapy. Because the drug is excreted
unchanged by the kidneys, careful monitoring of renal function is required. Dose adjustment should
be guided by estimated glomerular filtration rate, with discontinuation recommended when renal
function declines below established safety thresholds.
