Post-transplant hyperglycaemia: a study of risk factors

Mathew, Jayant T.; Rao, M Gopal; Job, Victoria; Ratnaswamy, Selvakumar; Jacob, C. K.

doi:10.1093/ndt/18.1.164

Cited by 70 publications

(38 citation statements)

References 24 publications

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“…Van Hooff et al [17] evaluated the mechanisms of NODAT and concluded that CsA and tacrolimus tend to reduce insulin release, while concomitant use of corticosteroids increases insulin resistance. A dose-response relationship between corticosteroids and NODAT has been demonstrated in some studies [17,18] but not in others [19,20]. In our study, differences in mean steroid and CsA doses (mg/kg/day) in the first 3 months were not statistically significant between groups.…”

Section: Discussioncontrasting

confidence: 72%

Endothelial nitric oxide synthase gene intron 4 polymorphism predicts new onset diabetes mellitus after transplantation in kidney allograft recipients treated with cyclosporin A

et al. 2010

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Section: Discussioncontrasting

confidence: 72%

Endothelial nitric oxide synthase gene intron 4 polymorphism predicts new onset diabetes mellitus after transplantation in kidney allograft recipients treated with cyclosporin A

et al. 2010

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“…Age was also a factor in a retrospective study of 939 kidney transplant recipients wherein PTDM increased mortality in those less than 55 years of age, but not in those over 55, compared to non-PTDM (141). Awareness of the potential impact of post-transplant diabetes increased even more with the study by Cosio et al (142), who described a 2-fold increase in mortality (Figure 4) compared to nontransplant recipients, which was equal to that of pretransplant diabetes, already established to worsen outcome, and independent of other factors known to reduce survival, and was confirmed by Kaskiske et al and others (33,34,142,143). The reduction in patient survival due to PTDM is largely attributable to increased cardiovascular disease events (33), as much as 3-fold even when controlling for other risk factors (144 -146).…”

Section: B Kidney Transplant Outcomesmentioning

confidence: 79%

“…Corticosteroids are well established to cause hyperglycemia through several mechanisms: by inducing or worsening pre-existing insulin resistance, increasing hepatic gluconeogenesis, and long-term, by stimulating appetite and weight gain (33)(34)(35). The impact is dose-dependent.…”

Section: Role Of Immunosuppression Agentsmentioning

confidence: 99%

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

Shivaswamy

Boerner

Larsen³

2015

Endocrine Reviews

250

203

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and VA Nebraska-Western Iowa Health Care System (V.S.), Omaha, Nebraska 68105Post-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. (Endocrine Reviews 37: 37-61, 2016)

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“…In another study, by taking a screening FBG level of 99 mg/dl (5.5 mmol/L) as a threshold for performing an OGTT, 90% of patients with newly diabetes and 78% of patients with dysglycemia were detected (38). In RTR, although 2HBG has been used to assess both the prevalence of PTD and IGT and changing glucose tolerance over time (1,22,40,41), no studies to date have examined the relationship between FBG and 2HBG. In this study, the FBG that gave the optimal sensitivity and specificity for predicting PTD was 101 mg/dl (5.6 mmol/L).…”

Section: Relationship Between Fbg and 2hbg In Rtrmentioning

confidence: 99%

Should an Oral Glucose Tolerance Test Be Performed Routinely in All Renal Transplant Recipients?

Armstrong

Prins

Beller

et al. 2006

Clinical Journal of the American Society of Nephrology

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Posttransplantation diabetes (PTD) contributes to cardiovascular disease and graft loss in renal transplant recipients (RTR). Current recommendations advise fasting blood glucose (FBG) as the screening and diagnostic test of choice for PTD. This study sought to determine (1) the predictive power of FBG with respect to 2-h blood glucose (2HBG) and (2) the prevalence of PTD using FBG and 2HBG compared with that using FBG alone, in prevalent RTR. A total of 200 RTR (mean age 52 yr; 59% male; median transplant duration 6.6 yr) who were >6 mo posttransplantation and had no known history of diabetes were studied. Patients with FBG <126 mg/dl (7.0 mmol/L; n ‫؍‬ 188) underwent an oral glucose tolerance test (OGTT). Receiver operating characteristic analyses evaluated the optimal level of FBG predictive of PTD (2HBG >200 mg/dl [11.1 mmol/L]) and impaired glucose tolerance (IGT; 2HBG 140 to 200 mg/dl [7.8 to 11.0 mmol/L]). An abnormal OGTT was reported in 79 (42%) nondiabetic RTR: PTD (n ‫؍‬ 22) and IGT (n ‫؍‬ 57). The optimal FBG that was predictive of PTD was 101 mg/dl (5.6 mmol/L; area under the curve 0.70; sensitivity 64%, specificity 67%, positive predictive value 20%, negative predictive value 93%). The optimal FBG that was predictive of IGT was less well defined (area under the curve 0.54). The prevalence of PTD was higher by OGTT than by FBG alone (17 versus 6%; P < 0.001). FBG may not be the optimal screening or diagnostic tool for PTD or IGT in RTR. Consideration should be given to introducing the OGTT as a routine posttransplantation investigation, although the implications of a pathologic OGTT are still to be determined in this population.

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Post-transplant hyperglycaemia: a study of risk factors

Cited by 70 publications

References 24 publications

Endothelial nitric oxide synthase gene intron 4 polymorphism predicts new onset diabetes mellitus after transplantation in kidney allograft recipients treated with cyclosporin A

Endothelial nitric oxide synthase gene intron 4 polymorphism predicts new onset diabetes mellitus after transplantation in kidney allograft recipients treated with cyclosporin A

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

Should an Oral Glucose Tolerance Test Be Performed Routinely in All Renal Transplant Recipients?

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