The association of early post-transplant glucose levels with long-term mortality

Valderhaug, Tone Gretland; Hjelmesæth, Jøran; Hartmann, Anders; Røislien, Jo; Bergrem, Harald; Leivestad, Torbjørn; Line, Pål–Dag; Jenssen, Trond

doi:10.1007/s00125-011-2105-9

Cited by 142 publications

(127 citation statements)

References 34 publications

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“…[17][18][19][20][21] As a consequence, a paradigm shift of treatment recommendations regarding changes in glucose metabolism in KTRs has been suggested. 22 Current investigations indeed have pointed toward a reduced risk of NODAT on major adverse events, presumably due to more thorough blood glucose monitoring posttransplant.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Tillmann

Radtke²,

Rump³

et al. 2017

Exp Clin Transplant

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Objectives: This study investigated the effect of prediabetes in long-term deceased-donor renal transplant recipients regarding graft survival, graft function, and evolution of new-onset diabetes after transplant compared with a control group of graft recipients with normal glucose tolerance test results. Materials and Methods: This was a follow-up trial of 187 deceased-donor renal transplant recipients. Based on oral glucose tolerance test results, the cohort was divided into groups A and B, comprising individuals with normal glucose metabolism (n = 130, 69.9%) and individuals with prediabetes (n = 56, 30.1%). Data are shown as means ± standard errors. Results: Both groups showed similar total transplant survival (116.8 ± 5.4 vs 114.5 ± 7.4 mo; P = .742) and transplant survival measured since oral glucose tolerance test (58.5 ± 1.4 vs 59.5 ± 1.9 mo; P = .990, Mantel-Cox P = .943). Univariate and multivariate Cox regression analyses showed no association of prediabetes with graft loss. Transplant function changes were similar between cohorts (-3 ± 1 vs -5 ± 2 mL/min/1.73 m 2 body surface area, using the Chronic Kidney Disease Epidemiology Collaboration formula; P = .538). At 5-year follow-up, recipients with prediabetes had higher hemoglobin A1c than controls (5.99% ± 0.10% vs 5.67% ± 0.04%; P = .002). Prediabetes was associated with a 4.5-fold increased hazard of new-onset diabetes after transplant (P = .021). Conclusions: Prediabetes was associated with a 4.5-fold higher hazard ratio for new-onset diabetes after transplant but not with reduced graft function or survival.

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Section: Discussionmentioning

confidence: 99%

Untitled

Tillmann

Radtke²,

Rump³

et al. 2017

Exp Clin Transplant

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“…Inclusion criteria were as follows: adult renal transplant recipient, .1 year posttransplant with stable renal function (,20% deviation in serum creatinine within last 2 months), stable prednisolone dose (maximum 5 mg/day) over the last 3 months, and BMI in the range of 18.5 to 29.9 kg/m 2 . Exclusion criteria were severe liver disease, pancreatitis (chronic or acute), previous bowel resection, inflammatory bowel disease, malignancy (previous or actual), estimated glomerular filtration rate (eGFR) ,25 mL/min/1.73 m 2 , pregnancy, and breast-feeding. The patients were recruited from October 2014 to February 2015.…”

Section: Patientsmentioning

confidence: 99%

GLP-1 Restores Altered Insulin and Glucagon Secretion in Posttransplantation Diabetes

et al. 2016

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OBJECTIVEDevelopment of posttransplantation diabetes (PTDM) is characterized by reduced insulin secretion and sensitivity. We aimed to investigate whether hyperglucagonemia could play a role in PTDM and to examine the insulinotropic and glucagonostatic effects of the incretin hormone glucagon-like peptide 1 (GLP-1) during fasting and hyperglycemic conditions, respectively. RESEARCH DESIGN AND METHODSRenal transplant recipients with (n = 12) and without (n = 12) PTDM underwent two separate experimental days with 3-h intravenous infusions of GLP-1 (0.8 pmol/kg/min) and saline, respectively. After 1 h of infusion, a 2-h hyperglycemic clamp (fasting plasma glucose + 5 mmol/L) was established. Five grams of arginine was given as an intravenous bolus 10 min before termination of the clamp. RESULTSFasting concentrations of glucagon (P = 0.92) and insulin (P = 0.23) were similar between the groups. In PTDM patients, glucose-induced glucagon suppression was significantly less pronounced (maximal suppression from baseline: 43 6 12 vs. 65 6 12%, P < 0.001), while first-and second-phase insulin secretion were significantly lower. The PTDM group also exhibited a significantly lower insulin response to arginine (P = 0.01) but similar glucagon and proinsulin responses compared with control subjects. In the preclamp phase, GLP-1 lowered fasting plasma glucose to the same extent in both groups but reduced glucagon only in PTDM patients. During hyperglycemic clamp, GLP-1 reduced glucagon concentrations and increased first-and second-phase insulin secretion in both groups. CONCLUSIONSPTDM is characterized by reduced glucose-induced insulin secretion and attenuated glucagon suppression during a hyperglycemic clamp. Similar to the case in type 2 diabetes, GLP-1 infusion seems to improve (insulin) or even normalize (glucagon) these pathophysiological defects.In renal transplant recipients, cardiovascular disease persists as the leading cause of premature death (1). Development of posttransplantation diabetes (PTDM) is associated with further increased cardiovascular risk and mortality (2-4). PTDM is primarily believed to be a variant of type 2 diabetes possibly induced by immunosuppressive therapy (5) and/or viral infections (e.g., cytomegalovirus and hepatitis C) that reduce both insulin secretion and insulin sensitivity (6). Importantly, the risk of PTDM can be significantly reduced by proper dosing of the immunosuppressive

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“…With strict definition for new onset diabetes, the tacrolimus-associated incidence is in excess of 30% in kidney recipients and even higher in liver recipients (First et al 2013). The degree of posttransplant hyperglycemia is predictive of cardiovascular and all-cause mortality (Valderhaug et al 2011). …”

Section: Why Is Tolerance Important?mentioning

confidence: 99%

Tolerance--Is It Worth It?

Finger

Strom

Matas

2013

Cold Spring Harbor Perspectives in Medicine

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We are entering an exciting time in the study of immunologic tolerance. Several cellular and molecular strategies have been developed that show promise in nonhuman transplant models and these approaches are just now appearing in clinical trials. Tolerance strategies that prevent immune rejection and obviate the need for immunosuppressive medications (with inherent risk of cancer, infection, and organ toxicity) would improve both graft and patient survival. Each tolerance protocol brings its own set of associated risks. As the results of these trials become available, we must continue to evaluate their successes and failures. The balance of these outcomes will help us answer the question: "Tolerance-Is it worth it?"WHAT IS TOLERANCE?

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The association of early post-transplant glucose levels with long-term mortality

Cited by 142 publications

References 34 publications

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GLP-1 Restores Altered Insulin and Glucagon Secretion in Posttransplantation Diabetes

Tolerance--Is It Worth It?

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