New-onset diabetes after transplantation (NODAT) is a frequent condition associated with a poor outcome. In kidney transplantation, hypomagnesemia is a frequent posttransplant complication and has been associated with calcineurin inhibitors use. Previous studies have analyzed the relationship between posttransplant hypomagnesemia and the risk of NODAT and provided conflicting conclusions. We conducted an observational study to analyze the relationship between pretransplant magnesemia (Mg) and the risk of NODAT within the first year of kidney transplantation.
A cohort study was conducted to determine the risk conferred by pretransplant magnesium level on development of NODAT within 1 year posttransplant. First time kidney transplant recipients between January 2005 and December 2010 with more than 6 months of follow-up were included. Mg was measured within the 24 hours preceding kidney transplantation. NODAT was defined according to the American Diabetes Association criteria.
Among the 154 patients analyzed, 28 (18.2%) developed NODAT at year 1. NODAT patients had lower levels of pretransplant Mg as compared with non-NODAT patients (P<0.02). When patients were divided into tertiles of Mg level, NODAT developed more frequently in patients in the lower tertile (Mg <2 mg/dL) as compared with patients in the higher tertile (Mg >2.3 mg/dL) (log rank, P<0.05). A multivariate analysis after adjustment to several variables demonstrated pretransplant Mg to be an independent risk factor of NODAT.
This study supports that a low pretransplant Mg level is an independent risk factor of NODAT in kidney transplant recipients.
Supplemental digital content is available in the article.
1 LUNAM Université, Angers, France.
2 Université Angers, CHU Angers, Service de Néphrologie-Dialyse-Transplantation, Angers, France.
3 Université Angers, CHU Angers, Service d’Onco-Pédiatrie, Angers, France.
4 Université Angers, CHU Angers, Département d’Anesthésie et Réanimation, Angers, France.
5 Université Angers, CHU Angers, Département de Chirurgie Vasculaire, Angers, France.
6 Université Angers, CHU Angers, Département de Pathologie Cellulaire et Tissulaire, Angers, France.
7 INSERM CIE5, Hopital Robert Debré, Paris, France.
8 Address correspondence to: Jean-François Augusto, M.D., Service de Néphrologie-Dialyse-Transplantation, CHU d’Angers, 49933 Angers Cedex 9, France.
The authors declare no funding or conflicts of interest.
J.-F.A. participated in conducting the study and writing the manuscript. J.-F.S. participated in revising the manuscript. A.D. participated in collecting the data of the study and revising the manuscript. J.R. participated in the statistical analysis. C.D., J.P., A.C., F.V., and C.O. participated in patient care and in revising the manuscript. J.S. participated in conducting the study and writing the manuscript.
Supplemental digital content (SDC) is available for this article. Direct URL citations appear in the printed text, and links to the digital files are provided in the HTML text of this article on the journal’s Web site (www.transplantjournal.com).
Received 12 April 2013. Revision requested 2 May 2013.
Accepted 11 November 2013.