Format

Send to

Choose Destination
Nat Rev Nephrol. 2015 Aug;11(8):465-77. doi: 10.1038/nrneph.2015.59. Epub 2015 Apr 28.

Emerging treatments for post-transplantation diabetes mellitus.

Author information

1
Research Group of Nephrology and Metabolism, Department of Clinical Medicine, UIT Arctic University of Norway, Hansine Hansens Veg 18, PO Box 6050 Langnes, 9037 Tromsø, Norway.
2
Department of Transplant Medicine, Section of Nephrology, Oslo University Hospital Rikshospitalet, Sognsvannvegen 20, PO Box 4950, Nydalen, Oslo 0424, Norway.

Abstract

Post-transplantation diabetes mellitus (PTDM), also known as new-onset diabetes mellitus (NODM), occurs in 10-15% of renal transplant recipients and is associated with cardiovascular disease and reduced lifespan. In the majority of cases, PTDM is characterized by β-cell dysfunction, as well as reduced insulin sensitivity in liver, muscle and adipose tissue. Glucose-lowering therapy must be compatible with immunosuppressant agents, reduced glomerular filtration rate (GFR) and severe arteriosclerosis. Such therapy should not place the patient at risk by inducing hypoglycaemic episodes or exacerbating renal function owing to adverse gastrointestinal effects with hypovolaemia. First-generation and second-generation sulphonylureas are generally avoided, and caution is currently advocated for the use of metformin in patients with GFR <60 ml/min/1.73 m(2). DPP-4 inhibitors do not interact with immunosuppressant drugs and have demonstrated safety in small clinical trials. Other therapeutic options include glinides and glitazones. Evidence-based treatment regimens used in patients with type 2 diabetes mellitus cannot be directly implemented in patients with PTDM. Studies investigating the latest drugs are required to direct the development of improved treatment strategies for patients with PTDM. This Review outlines the modern principles of glucose-lowering treatment in PTDM with specific reference to renal transplant recipients.

PMID:
25917553
DOI:
10.1038/nrneph.2015.59
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center