Unmasking Glucose Metabolism Alterations in Stable Renal Transplant Recipients

Delgado, Patricia; Dı́az, Juan; Silva, Irene; Osorio, J.M.; Osuna, Antonio; Bayés, Beatriz; Lauzurica, Ricardo; Arellano, Edgar Marcelo; Campistol, J. M.; Domínguez, Rosa; Gómez-Alamillo, C.; Ibernón, Meritxell; Moreso, Francesc; Benı́tez, Rocı́o; Lampreave, Ildefonso; Porrini, Esteban; Torres, Armando

doi:10.2215/cjn.04921107

Cited by 23 publications

(19 citation statements)

References 19 publications

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“…Overall, the reported prevalence of abnormal glucose metabolism was remarkably similar to the present results and ranged from 32 (28) to 51% (27). Our previous OGTT-based analysis of TIP study control patients at 3 months posttransplantation, however, showed 84% abnormal glucose metabolism, with 52% NODAT (16).…”

Section: Discussionsupporting

confidence: 89%

Glucose Metabolism After Renal Transplantation

et al. 2013

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OBJECTIVEWe determined prevalence, risk factors, phenotype, and pathophysiological mechanism of new-onset diabetes after transplantation (NODAT) to generate strategies for optimal pharmacological management of hyperglycemia in NODAT patients.RESEARCH DESIGN AND METHODSRetrospective cohort study comparing demographics, laboratory data, and oral glucose tolerance test (OGTT)-derived metabolic parameters from kidney transplant recipients versus subjects not receiving transplants.RESULTSAmong 1,064 stable kidney transplant recipients (≥6 months posttransplantation), 113 (11%) had a history of NODAT and 132 (12%) had pretransplant diabetes. In the remaining patients, randomly assigned OGTTs showed a high prevalence of abnormal glucose metabolism (11% diabetes; 32% impaired fasting glucose, impaired glucose tolerance, or both), predominantly in older patients who received tacrolimus as the primary immunosuppressant. Compared with 1,357 nontransplant subjects, stable kidney transplant recipients had lower basal glucose, higher glycated hemoglobin, lower insulin secretion, and greater insulin sensitivity in each of the three subgroups, defined by OGTT 2-h glucose (<140, 140–199, ≥200 mg/dL). These findings were reinforced in linear spline interpolation models of insulin secretion and sensitivity (all P < 0.001) and in another regression model in which the estimated oral glucose insulin sensitivity index was substantially higher (by 79–112 mL/min m2) for transplant versus nontransplant subjects despite adjustments for age, sex, and BMI (all P < 0.001).CONCLUSIONSGlucose metabolism differs substantially between kidney transplant recipients and nontransplant controls. Because impaired insulin secretion appears to be the predominant pathophysiological feature after renal transplantation, early therapeutic interventions that preserve, maintain, or improve β-cell function are potentially beneficial in this population.

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Section: Discussionsupporting

confidence: 89%

Glucose Metabolism After Renal Transplantation

et al. 2013

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“…Thus, only FPG was considered, and previous studies showed that postprandial hyperglycemia is common after transplantation even in patients with normal FPG (19). Perhaps, glycated hemoglobin may be a better marker of CV risk than FPG levels in transplant patients (20, 21), but unfortunately, this parameter was not available for analysis.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Consequences of New-Onset Hyperglycemia After Kidney Transplantation

et al. 2012

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Background New-onset diabetes after transplantation (NODAT) is associated with high cardiovascular (CV) risk and reduced patient survival. It is unclear whether this risk is newly acquired or represents preexisting CV disease in patients with this complication. Methods Included are 1146 adults, recipients of first kidney transplants from 1984 to 2008 treated with modern immunosuppressants. Results One year after transplantation, 29.8% of patients experienced impaired fasting glycemia and 13.4% NODAT. The risk of NODAT related to recipient variables include the following: older age, male gender, higher body mass index, higher pretransplantation glucose and triglyceride levels, and lower high-density lipoprotein level. Increasing fasting glucose levels at 1, 4, or 12 months after transplantation, independent of other factors, related to reduced patient survival (12 months hazard ratio [HR]=1.146 [1.132–1.161], P<0.0001 for 10mg/dL increase in glucose), and this was primarily because of an increase in CV deaths. Hyperglycemia related to all major CV events (MCVE), cardiac (HR=1.113 [1.094–1.132], P<0.0001), vascular (HR=1.168 [1.140–1.197], P<0.0001), and strokes (HR=1.156 [1.123–1.191], P=0.003). These relations were statistically independent of other risk factors. The increased risk of MCVE was noted particularly in patients without MCVE before transplantation (HR=1.145 [1.126–1.165], P<0.0001). Furthermore, among patients with after transplantation MCVE (n=123, 11%), hyperglycemia increases the risk of death (NODAT: HR=2.410 [1.125–5.162], P=0.024). Conclusions After transplantation hyperglycemia is a strong independent risk factor for MCVE and death, mainly from CV causes. This risk is independent of the presence of CV disease identified before transplantation.

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“…Additional measures to improve cardiovascular outcomes include oral glucose tolerance tests to diagnose impaired glucose metabolism adequately, and strict glucose control to reduce the risks associated with hyperglycemia and NODAT [46]. Sharif et al .…”

Section: Strategies To Minimize Cardiovascular Riskmentioning

confidence: 99%

Risk factors for cardiovascular disease in renal transplant recipients and strategies to minimize risk

Liefeldt¹,

Budde²

2010

Transplant International

106

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Summary Cardiovascular disease is the leading cause of death following renal transplantation, and renal transplant patients have a greatly increased cardiac risk compared with the general population. Death with a functioning graft caused by cardiovascular disease also represents a substantial cause of graft loss. Decreased renal function in transplant recipients is a major contributor to increased cardiac risk, both as an independent risk factor and because of its negative effects on hypertension, anemia, left ventricular hypertrophy, and dyslipidemia. Graft loss and diabetes mellitus are also significant risk factors for cardiac death. Although critical for maintaining the transplanted organs, standard immunosuppressants have toxicities that exacerbate cardiac risk. Preservation of renal function, prevention of graft loss, and reductions in cardiovascular risk factors via improvements in both patient management and immunosuppressive therapies constitute critical strategies for optimizing patient and graft survival over the long term.

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Unmasking Glucose Metabolism Alterations in Stable Renal Transplant Recipients

Cited by 23 publications

References 19 publications

Glucose Metabolism After Renal Transplantation

Glucose Metabolism After Renal Transplantation

Cardiovascular Consequences of New-Onset Hyperglycemia After Kidney Transplantation

Risk factors for cardiovascular disease in renal transplant recipients and strategies to minimize risk

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