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Retrospective cohort study shows increased risk of diabetes in renal transplant recipients, suggesting vital metabolic assessments.
Background/Introduction Post-transplant diabetes mellitus (PTDM) is a common complication in renal transplant recipients. We aimed to investigate changes in fasting plasma glucose (FPG) and HbA1c levels following renal transplantation in non- diabetic patients and explore associations with metabolic risk factors, immunosuppressive therapy, and liver fibrosis scores. Methods This retrospective cohort study included 200 patients who underwent renal transplantation between 2011 and 2024 without preexisting diabetes. FPG and HbA1c were recorded pre-transplant and at 3, 6, and 12 months post-transplant. NAFLD Fibrosis Score (NFS) and Fibrosis-4 (FIB-4) were calculated postoperatively. Data on demographics, BMI, comorbidities, immunosuppressive regimens, graft rejection, and survival were collected. Results Renal transplantation led to a clinically relevant increase in glycaemic parameters, with median FPG rising from 89.5 mg/dl preoperatively to 108 mg/dl postoperatively (p<0.001). Post-transplant diabetes mellitus (PTDM) developed in 30.5% of previously non-diabetic patients, underlining the metabolic burden of immunosuppressive therapy.Older age and higher BMI emerged as strong, independent risk factors for PTDM. Diabetic patients were on average 15 years older than their non-diabetic counterparts (p<0.001), and had significantly higher BMI (26.8 ± 4.9 vs 24.5 ± 4.6, p<0.05).Male recipients showed a higher rate of overt diabetes (37.6% vs 23.5%), while females more frequently developed prediabetes (43.1% vs 30.9%).Notably, postoperative FPG showed a significant positive correlation with liver fibrosis scores (NFS and FIB-4; r=0.167-0.277, p<0.05), suggesting that subclinical hepatic dysfunction and insulin resistance may share a common pathophysiological axis post-transplant. Conclusion(s) Renal transplantation in non-diabetic patients is associated with a marked deterioration in glycaemic control, with nearly one-third developing PTDM within the first year. Advancing age and elevated BMI significantly increase susceptibility, highlighting the urgent need for pre-emptive metabolic risk stratification.The observed sex-specific glycaemic responses suggest underlying biological differences in post-transplant glucose metabolism, warranting further investigation. Moreover, the significant correlation between glycaemic markers and liver fibrosis indices underscores a potential metabolic-hepatic interplay, driven by insulin resistance and immunosuppressive exposure. Optimization of immunosuppressive regimens and lifestyle interventions could prove pivotal in reducing the burden of PTDM and enhancing long-term transplant success.
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Simsek et al. (2025) studied this question.
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