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Can We Predict New-Onset Diabetes After Transplantation Previously?

R. Imamura,1 K. Tsutahara,2 S. Nakazawa,1 Y. Kakuta,1 T. Abe,1 T. Takao,2 N. Ichimaru,3 S. Yamaguchi,2 S. Takahara,3 N. Nonomura.1

1Urology, Osaka University Graduate School of Medicine, Suita, Japan
2Urology, Osaka General Medical Center, Osaka, Japan
3Advanced Technology for Transplantation, Osaka University Graduate School of Medicine, Suita, Japan.

Meeting: 2016 American Transplant Congress

Abstract number: A260

Keywords: FK506, Hyperglycemia, Kidney transplantation, Post-transplant diabetes

Session Information

Date: Saturday, June 11, 2016

Session Name: Poster Session A: Poster Session III: Kidney Complications-Other

Session Time: 5:30pm-7:30pm

 Presentation Time: 5:30pm-7:30pm

Location: Halls C&D

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Objectives: New-onset diabetes after transplantation (NODAT), one of the important complications after kidney

transplantation, leads to reduce graft survival rate and increase patient morbidity and mortality. Because of its high incidence of cardiovascular diseases, prevention of NODAT is strongly desirable. The aim of this study is to analyze the risk factors on the development of NODAT.

Methods: A retrospective analysis was performed on 43 kidney transplant recipients who are over 15 years old, serum creatinine<2.0 mg/dl at 12 month after kidney transplantation, and free of previously known diabetes. Maintenance immunosuppressive regimen consists of tacrolimus extended-release (TACER), mycophenolate mofetil, steroid with or without everolimus. Body mass index, blood pressure (office blood pressure only), laboratory parameters were measured before transplantation, 3 month and 12 month after transplantation. All patients were performed oral glucose tolerance tests before and after (3M and 12M) transplantation.

Results: The incidence rate of NODAT is 11.9% at 3M and 16.7% at 12M after kidney transplantation. It is suggested that male (3M and 12M), older (12M), pre-transplant IGT (12M), high systolic and diastolic blood pressure (12M) are risk factors of NODAT. In homeostasis model assessment ratio (HOMA-R), there was not significant difference between normal and NODAT groups. On the other hand, in insulinogenic index, NODAT group is significantly lower than normal group at both 3M and 12M. In multivariate analysis, homeostasis model assessment beta cell function (HOMA-beta) prior kidney transplantation was an independent factor predicting NODAT at 12M (p=0.0222, OR=0.95 vs normal group).

Conclusions: The incidence rate of NODAT was under 20% in the patients using tacrolimus extended-release at the first year after kidney transplantation. HOMA-beta prior kidney transplantation was the most important risk factor on the development of NODAT in early period. To prevent NODAT not only short term but also long period, reducing the dose of both glucocorticoid and CNI (TACER) within the limit of preventing acute rejection may be important for the patients who don't have enough level of HOMA-beta prior kidney transplantation.

CITATION INFORMATION: Imamura R, Tsutahara K, Nakazawa S, Kakuta Y, Abe T, Takao T, Ichimaru N, Yamaguchi S, Takahara S, Nonomura N. Can We Predict New-Onset Diabetes After Transplantation Previously? Am J Transplant. 2016;16 (suppl 3).

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To cite this abstract in AMA style:

Imamura R, Tsutahara K, Nakazawa S, Kakuta Y, Abe T, Takao T, Ichimaru N, Yamaguchi S, Takahara S, Nonomura N. Can We Predict New-Onset Diabetes After Transplantation Previously? [abstract]. Am J Transplant. 2016; 16 (suppl 3). https://atcmeetingabstracts.com/abstract/can-we-predict-new-onset-diabetes-after-transplantation-previously/. Accessed February 25, 2021.

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