Nephrol Dial Transplant (2003) 18: 2154-2159
© 2003 European Renal Association-European Dialysis and Transplant Association
Original Article
A 6-year prospective study on new onset diabetes mellitus, insulin release and insulin sensitivity in renal transplant recipients
1Department of Medicine, Section of Nephrology and 2Department of Clinical Chemistry, Rikshospitalet, Oslo, Norway
Correspondence and offprint requests to: Monica Hagen, Department of Medicine, Section of Nephrology, Laboratory for Renal Physiology, Rikshospitalet, 0027 Oslo, Norway. Email: monica.hagen{at}rikshospitalet.no
Background. It is well known that both insulin resistance and insulin deficiency are involved in the pathogenesis of post-transplant diabetes mellitus (PTDM), but the relative importance of the two different mechanisms is still under debate. The present prospective longitudinal study was performed over 6 years to investigate the impact of impaired insulin secretion (ISec) and insulin sensitivity (IS) in the development of PTDM in renal transplant recipients.
Methods. A total of 95 non-diabetic patients underwent a 75 g oral glucose tolerance test (OGTT) 10 weeks post-transplant. Six years later, 63 of these recipients were re-examined, the majority (n = 58) with an OGTT. Fasting, 1- and 2-h insulin and glucose levels were measured and used to estimate the insulin secretory response and IS both at baseline and at follow-up.
Results. The proportion of recipients with normal glucose tolerance (NGT) rose from 46% (baseline) to 65% (follow-up) (P = 0.008), and median fasting and 2-h serum glucose were reduced by 0.7 mmol/l (P < 0.001) and 1.3 mmol/l (P = 0.039), respectively. The recipients with PTDM at follow-up had a significant decline in the estimated median first and second phase ISec (–58 and –47%, respectively, P = 0.005 for both). The patients who normalized their glucose tolerance from PTDM or IGT at baseline to NGT at follow-up increased their IS significantly (68%, P = 0.002) without significant alterations in ISec.
Conclusions. Impaired ISec seems to be the dominant mechanism in the development of PTDM after renal transplantation. In contrast, normalization of glucose intolerance is associated with improved IS.
Keywords: insulin release; insulin sensitivity; post-transplant diabetes mellitus; renal transplantation
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