Hyperglycaemia following a simultaneous pancreas and kidney transplant

A 46-year-old Black British man attended transplant follow-up. He had a history of Type 1 diabetes (T1D) diagnosed at the age of 14, with modest glucose control. He developed significant diabetic nephropathy progressing to severe chronic kidney disease and underwent pre-emptive simultaneous pancreas and kidney (SPK) transplantation 6 years previously. Transplant renal function was good and regular glycated haemoglobin tests were normal (36–41 mmol/mol [5.6%–5.9%]). At his most recent transplant clinic visit, his glycated haemoglobin had risen to 72 mmol/mol (8.7%). He was assessed urgently in the renal transplant diabetes clinic. His immunosuppression treatments were tacrolimus, mycophenolate mofetil and prednisolone 5 mg daily at stable doses over the preceding months. What are the potential reasons for hyperglycaemia following SPK transplantation? What investigations are required? He was asymptomatic, but home capillary blood glucose tests ranged from 5.6 mmol/L–13.6 mmol/L. Blood tests showed a normal serum lipase, a C-peptide of 899 pmol/L (paired glucose 7.9 mmol/L) and weakly positive glutamic acid decarboxylase antibodies at a titre of 21 units/L (normal <6). He was noted to have had a 25 kg weight gain following the transplant, with a current body mass index of 32.5 kg/m2. His case was discussed with the transplant surgical team who undertook an urgent pancreatic biopsy. This showed no evidence of rejection but did show evidence of recurrent T1D, with insulitis affecting many islets. The clinical impression was that his hyperglycaemia was likely due to a combination of recurrent autoimmunity, with resultant loss of insulin secretion, which was exacerbated by insulin resistance due to significant weight gain (plus the impact of immunosuppression). He was commenced on metformin, but was unable to tolerate it and subsequently commenced on dulaglutide. He achieved 7 kg weight loss, and glycated haemoglobin has remained around 46–47 mmol/mol (6.3%–6.4%). His C-peptide has remained around 1000 pmol/L. Hyperglycaemia following SPK transplantation is important and requires investigation. The most important cause is rejection.1 Weight gain following SPK transplantation, however, is common.2 Hyperglycaemia may, therefore, also occur due to insulin resistance, or the effect of immunosuppressants such as steroids and calcineurin inhibitors. Recurrent T1D in a transplanted pancreas is rare. In a Spanish case series of 81 participants with pancreas transplants, only two participants developed recurrent T1D.3 Rates of pancreas graft survival post-SPK transplant are currently quoted at 86% at 1 year and 53% at 10 years.4 Mitigating weight gain is an important aim post-SPK transplantation and may aid the longevity of the pancreas graft. If there are symptoms of hyperglycaemia or insulin deficiency post-SPK, prompt use of insulin pending investigations is advised to reduce the risk of hyperglycaemic emergency. The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

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