J Investig Med. 2010 Aug;58(6):755-63. doi: 10.231/JIM.0b013e3181e61a64.
Journal of investigative medicine : the official publication of the American Federation for Clinical Research
Pablo F Mora
PMID: 20517164 DOI: 10.231/JIM.0b013e3181e61a64
Transplantation medicine has grown to be an important element of medical practice, and with the development of modern immunosuppression agents and protocols, the occurrence of diabetes as renal transplantation is recognized as one of the metabolic consequences of therapy with these agents. New-onset diabetes after transplantation can be defined as diabetes mellitus developing in any patient without history of diabetes before transplantation, who has sustained hyperglycemia that meets the current diagnostic criteria by the American Diabetes Association or by the World Health Organization. New-onset diabetes after transplantation has been associated with the following risk factors: age, non-white ethnicity, hepatitis C infection, glucocorticoid therapy for rejection, and chronic immunosuppression with cyclosporine and tacrolimus. The observation that current immunosuppression using tacrolimus is one of the most important single risk factor for the development of new-onset diabetes after transplantation has been made. The pathophysiology of this condition resembles that of type 2 diabetes mellitus. There is conclusive evidence that pretransplantation end-stage renal disease is an insulin-resistant state, and after transplantation, glucocorticoids induce further peripheral insulin insensitivity. The "second hit" seems to be an acquired (yet reversible) insulin secretion defect caused by the calcineurin inhibitors cyclosporine but more pronounced with tacrolimus. Future directions include pretransplantation and posttransplantation testing using glucose measurements and other techniques to identify high-risk individuals and possibly develop treatment strategies aimed to modify insulin resistance as well as to preserve beta cell function.
