Abstract: TH-PO151
Glucose Metabolism After Renal Transplantation: Oral Glucose Tolerance Test-Derived Insulin Release and Insulin Sensitivity Under Tacrolimus versus Belatacept-Based Immunosuppression
Session Information
- Transplantation: Cardiovascular and Metabolic Diseases
October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 1802 Transplantation: Clinical
Authors
- Hecking, Manfred, Medical University of Vienna, Nephrology & Dialysis, Vienna, Austria
- Müller, Martin, Medical University of Vienna, Vienna, Austria
- Haidinger, Michael, Medical University of Vienna, Vienna, Austria
- Schwaiger, Elisabeth, Medical University Vienna, Vienna, Austria
- Pacini, Giovanni, Institute of Neuroscience, National Research Council, Padova, Italy
- Tura, Andrea, CNR Institu of Neuroscience, Padova, Italy
- Werzowa, Johannes, Medical University of Vienna, Vienna, Austria
- Saemann, Marcus D., Wilhelminen Hospital, Vienna, Austria
Background
In our previous oral glucose tolerance test (OGTT)-based study (PMID23656979), calcineurin inhibitor-treated kidney transplant recipients (KTRs) showed lower insulin release but higher insulin sensitivity than non-KTRs. We aimed at refining our analysis, using only Tacrolimus-treated KTRs (Tac-KTRs) vs Belatacept-treated KTRs (Bela-KTRs) as controls.
Methods
We revisited our database and analysed indices of insulin release and insulin sensitivity from OGTTs of 67 Tac- vs 26 Bela-KTRs.
Results
Our center’s outpatient records showed 38 Tac-KTRs vs 0 Bela-KTRs among 113 KTRs with treated posttransplant diabetes mellitus. The randomly assigned OGTTs among KTRs with unknown glycemic status differed between Tac- vs Bela-KTRs: 11 vs 0 diabetics (2-h glucose [2-h G] ≥200 mg/dL), 24 vs 2 prediabetics (2-h G 140-199) and 32 vs 24 with normal glucose tolerance (NGT) (2-h G <140) [p<0.01]. Tac- vs Bela-KTRs with NGT had similar age, body mass index, 0-h and 2-h G, but higher HbA1c and insulin sensitivity and lower insulin release (Table and Figure).
Conclusion
In line with our previous study, impaired insulin release was the main pathophysiological feature for diabetes development in Tac-KTRs, while Bela-KTRs had no impaired glucose metabolism. It is tempting to speculate that impaired insulin secretion, due to beta-cell damage, in Tac-KTRs is compensated by increased insulin sensitivity, but this mechanism seems more complex and deserves further study.