Glucometabolism in kidney transplant recipients with and without posttransplant diabetes: Focus on beta-cell function

Kurnikowski, Amelie; Salvatori, Benedetta; Krebs, Michael; Budde, Klemens; Eller, Kathrin; Pascual Santos, Julio; Morettini, Micaela; Göbl, Christian; Hecking, Manfred; Tura, Andrea

doi:http://dx.doi.org/10.3390/biomedicines12020317

Glucometabolism in kidney transplant recipients with and without posttransplant diabetes: Focus on beta-cell function

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Kurnikowski A, Salvatori B, Krebs M, Budde K, Eller K, Pascual J, et al. Glucometabolism in kidney transplant recipients with and without posttransplant diabetes: Focus on beta-cell function. Biomedicines. 2024 Jan 30;12(2):317. DOI: 10.3390/biomedicines12020317

Abstract

Posttransplant diabetes mellitus (PTDM) is a common complication after kidney transplantation. Pathophysiologically, whether beta-cell dysfunction rather than insulin resistance may be the predominant defect in PTDM has been a matter of debate. The aim of the present analysis was to compare glucometabolism in kidney transplant recipients with and without PTDM. To this aim, we included 191 patients from a randomized controlled trial who underwent oral glucose tolerance tests (OGTTs) 6 months after transplantation. We derived several basic indices of beta-cell function and insulin resistance as well as variables from mathematical modeling for a more robust beta-cell function assessment. Mean ± standard deviation of the insulin sensitivity parameter PREDIM was 3.65 ± 1.68 in PTDM versus 5.46 ± 2.57 in NON-PTDM. Model-based glucose sensitivity (indicator of beta-cell function) was 68.44 ± 57.82 pmol∙min-1∙m-2∙mM-1 in PTDM versus 143.73 ± 112.91 pmol∙min-1∙m-2∙mM-1 in NON-PTDM, respectively. Both basic indices and model-based parameters of beta-cell function were more than 50% lower in patients with PTDM, indicating severe beta-cell impairment. Nonetheless, some defects in insulin sensitivity were also present, although less marked. We conclude that in PTDM, the prominent defect appears to be beta-cell dysfunction. From a pathophysiological point of view, patients at high risk for developing PTDM may benefit from intensive treatment of hyperglycemia over the insulin secretion axis.