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Review
. 2016 Feb;37(1):37-61.
doi: 10.1210/er.2015-1084. Epub 2015 Dec 9.

Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes

Affiliations
Review

Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes

Vijay Shivaswamy et al. Endocr Rev. 2016 Feb.

Abstract

Post-transplant diabetes mellitus (PTDM) is a frequent consequence of solid organ transplantation. PTDM has been associated with greater mortality and increased infections in different transplant groups using different diagnostic criteria. An international consensus panel recommended a consistent set of guidelines in 2003 based on American Diabetes Association glucose criteria but did not exclude the immediate post-transplant hospitalization when many patients receive large doses of corticosteroids. Greater glucose monitoring during all hospitalizations has revealed significant glucose intolerance in the majority of recipients immediately after transplant. As a result, the international consensus panel reviewed its earlier guidelines and recommended delaying screening and diagnosis of PTDM until the recipient is on stable doses of immunosuppression after discharge from initial transplant hospitalization. The group cautioned that whereas hemoglobin A1C has been adopted as a diagnostic criterion by many, it is not reliable as the sole diabetes screening method during the first year after transplant. Risk factors for PTDM include many of the immunosuppressant medications themselves as well as those for type 2 diabetes. The provider managing diabetes and associated dyslipidemia and hypertension after transplant must be careful of the greater risk for drug-drug interactions and infections with immunosuppressant medications. Treatment goals and therapies must consider the greater risk for fluctuating and reduced kidney function, which can cause hypoglycemia. Research is actively focused on strategies to prevent PTDM, but until strategies are found, it is imperative that immunosuppression regimens are chosen based on their evidence to prolong graft survival, not to avoid PTDM.

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Figures

Figure 1.
Figure 1.
Total solid organ transplants performed in the United States. Numbers represent transplants performed from January 1988 to March 31, 2015, and reported to the United Network for Organ Sharing.
Figure 2.
Figure 2.
Potential contributors to PTDM. Risk factors for PTDM including pre-existing diabetes risk, immunosuppressant agents used for treatment, inflammation, and other factors. FH, family history; DM, diabetes; HDL, high-density lipoprotein; TX, transplant; Vit D, vitamin D; Mg, magnesium; HepC, hepatitis C.
Figure 3.
Figure 3.
Sirolimus and CNI impact on insulin signaling pathway. PDK1, phosphoinositide-dependent protein kinase 1; Rictor, rapamycin-insensitive companion of mTOR; Proctor, protein observed with Rictor; Raptor, regulatory-associated protein of mTOR; PRAS40, proline-rich Akt substrate 40; mLST8, mTOR-associated protein, LST8 homolog; YY1, Yin Yang 1; mSIN1, mammalian stress-activated protein kinase interactions protein; p, phosphorylation. Note that direct stimulation is denoted by formula image, inhibition is denoted by formula image, and tentative inhibition by formula image.
Figure 4.
Figure 4.
Impact of PTDM on kidney transplant survival. Kaplan-Meier patient survival in the three study groups: no diabetes (thin line), pretransplant diabetes (thick line), and PTDM (dashed line). A, Survival was calculated from the day of transplantation in all three groups of patients. B, For PTDM, survival was calculated from the time of development of diabetes, and for the other two groups, from the day of transplantation. [Reprinted from F. G. Cosio et al: Patient survival after renal transplantation: IV. Impact of post-transplant diabetes. Kidney Int. 2002;62:1440–1446 (142), with permission. © International Society of Nephrology.]

References

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