Background: A dysfunction of the HNF-1beta gene can lead to renal loss of magnesium, hyperuricemia and diabetes mellitus. There is a striking similarity between this clinical phenotype and the frequent occurrence of new-onset diabetes after transplantation (NODAT), hypomagnesaemia and hyperuricemia in organ transplant patients treated with tacrolimus. We therefore hypothesized that dysfunction of the HNF-1beta gene might be involved in the pathogenesis of NODAT in tacrolimus treated renal transplant patients.

Aim: To investigate whether NODAT, hypomagnesaemia and hyperuricemia are mutually associated in tacrolimus-treated renal transplant patients.

Patients and methods: We conducted a retrospective study in adult patients who received a living donor kidney between January 2006 and December 2011, and were treated with tacrolimus. NODAT was defined as a HbA1c level of > 7.0% or the use of hypoglycemic drugs. We excluded patients with a prior history of diabetes mellitus. Magnesium and urate levels were measured immediately before transplantation and 1 week post transplantation.

Results: Of the 263 patients, 53 (20.2%) developed NODAT within the first three months after transplantation. Patients without NODAT (n=210) served as controls. Both groups had a comparable dose of prednisone and tacrolimus at 3 months after transplantation. The BMI at the time of transplantation was significantly higher in the NODAT group (25.1±3.1 kg/m² versus 23.9±3.6 kg/m²; p< 0.05). Prior to transplantation, the magnesium and urate levels did not differ between the NODAT and the control group: 0.94±0.17 mmol/L versus 0.96±0.18 mmol/L and 0.34±0.13 mmol/L versus 0.33±0.10 mmol/L (NS). Although both the magnesium and urate levels were lower post transplantation, there was again no difference between the NODAT and control group: 0.77±0.16 mmol/L versus 0.77±0.14 mmol/L and 0.31±0.10 mmol/L versus 0.31±0.35 mmol/L. Logistic regression analysis did not reveal a relation between NODAT and magnesium or urate levels.

Conclusion: We found no evidence for a clustering of NODAT, hyperuricemia and hypomagnesaemia in tacrolimus treated renal transplant patients. Involvement of the HNF-1beta gene in the pathogenesis of NODAT is therefore unlikely.

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