Guideline narrative review discusses diabetes risks from immunosuppressive therapy in kidney transplant recipientsGuidelines address diabetes risks in kidney transplant patients

Post-transplant diabetes mellitus (PTDM) affects 7–39% of kidney transplant recipients and substantially worsens cardiovascular, infectious, and allograft outcomes. Although PTDM shares core pathophysiological features with type 2 diabetes—peripheral insulin resistance and impaired β-cell secretion—its etiology is fundamentally shaped by immunosuppressive therapy. Calcineurin inhibitors suppress insulin gene transcription via NFAT inhibition and exacerbate lipotoxicity; corticosteroids drive hepatic gluconeogenesis and impair GLUT4-mediated glucose uptake; and mTOR inhibitors reduce β-cell mass through mTORC1-dependent mechanisms. Chronic NF-κB/JNK-driven inflammation further amplifies insulin resistance and promotes β-cell apoptosis. Beyond these established mechanisms, we propose a unifying “gut–immune–metabolic axis” in which immunosuppression-induced gut microbiota dysbiosis—characterized by depletion of short-chain fatty acid-producing taxa (Roseburia, Faecalibacterium prausnitzii) and Akkermansia muciniphila—drives intestinal barrier dysfunction, endotoxemia, impaired FXR/TGR5-mediated GLP-1 secretion, and TMAO-associated metabolic inflammation, collectively perpetuating glucose dysregulation. Risk stratification integrates non-modifiable factors (advanced age, African American/Hispanic/South Asian ethnicity, TCF7L2 polymorphisms, autosomal dominant polycystic kidney disease) with modifiable determinants (pre-transplant dysglycemia, obesity, hypomagnesemia, hepatitis C and cytomegalovirus infections, acute rejection, and diuretic use). Diagnosis requires OGTT-centered assessment per the 2024 International Consensus guidelines, with cautious interpretation of HbA1c during the early post-transplant period. Management encompasses personalized immunosuppression (corticosteroid minimization, tacrolimus trough levels