, Volume 57, Issue 10, pp 2076–2080 | Cite as

Postoperative impaired glucose tolerance is an early predictor of pancreas graft failure

  • Shruti MittalEmail author
  • Myura Nagendran
  • Rachel H. Franklin
  • Edward J. Sharples
  • Peter J. Friend
  • Stephen C. L. Gough



The management of pancreatic transplantation is limited by a lack of clinically relevant early markers of graft dysfunction to enable intervention prior to irreversible damage. The aim of this study was to assess the OGTT as an early predictor of pancreatic graft failure.


Patients with graft failure (return to insulin dependence) were identified from a prospectively maintained clinical database. Data from OGTTs performed within 2 weeks of the transplant were retrospectively collected for 210 subjects, 42 with graft failure (21 after simultaneous pancreas–kidney transplant and 21 after isolated pancreas transplant) matched to 168 with functioning grafts. The groups were compared to assess the relationship between early OGTT result and pancreas graft failure.


Mean 2 h glucose from the OGTT was significantly higher in the overall graft failure group compared with the control group (8.36 vs 6.81 mmol/l, p = 0.014). When interpreted in combination with fasting glucose, abnormal glucose tolerance was more common in the failed graft group (50% vs 22%, p = 0.001). In an adjusted model, abnormal glucose tolerance emerged as the most predictive independent factor for graft failure, HR 1.66 (95% CI 1.22, 2.24), p = 0.001. These findings were consistent between the different transplant procedures performed.


We conclude that early post-transplant abnormal glucose tolerance is associated with later whole organ pancreas graft failure. An OGTT performed within the first month postoperatively provides an easily measurable assessment of an independent early risk factor of pancreatic graft dysfunction.


Metabolic biomarkers Pancreas transplant Risk factors Survival Transplant outcome Type 1 diabetes 



Cold ischaemia time


Isolated pancreas transplant


Simultaneous pancreas–kidney transplant



We would like to acknowledge our consultant colleagues at the Oxford Transplant Centre, R. Ploeg, A. Vaidya, S. Sinha, I. Quiroga, J. Gilbert and S. Reddy, who have contributed to the generation of this data.


The first author was funded through a Clinical Research Fellowship from the NIHR Biomedical Research Centre, Oxford.

Duality of interest

The authors of this manuscript have no conflicts of interest.

Contribution statement

All authors contributed to the concept and design of the study, acquisition of data, analysis and interpretation. All authors were involved in the preparation of the article draft and final version. SM is responsible for the integrity of the work as a whole.


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Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  • Shruti Mittal
    • 1
    • 2
    • 3
    Email author
  • Myura Nagendran
    • 4
  • Rachel H. Franklin
    • 1
  • Edward J. Sharples
    • 5
    • 6
  • Peter J. Friend
    • 1
    • 6
  • Stephen C. L. Gough
    • 3
    • 5
  1. 1.Oxford Transplant CentreChurchill HospitalOxfordUK
  2. 2.Nuffield Department of SurgeryUniversity of OxfordOxfordUK
  3. 3.NIHR Oxford Biomedical Research CentreOxfordUK
  4. 4.Green Templeton CollegeUniversity of OxfordOxfordUK
  5. 5.Oxford Centre for Diabetes, Endocrinology and MetabolismOxfordUK
  6. 6.Nuffield Department of MedicineUniversity of OxfordOxfordUK

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