89 research outputs found

    No evidence of association between NOD2/CARD15 gene polymorphism and atherosclerotic events after renal transplantation.

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    International audienceStable renal transplant recipients (RTR) display high rates of atherosclerotic events (AE). Innate immunity and especially vascular inflammation play a role in the pathogenesis of atherosclerosis. It is illustrated both by an increased occurrence of postrenal transplant cardiovascular events in patients with elevated levels of C-reactive protein and by a correlation between posttransplant AE and Toll-like receptor-4 Asp299Gly polymorphism. Here, we analyze the influence NOD2/CARD15 gene polymorphism since NOD2 can modulate macrophage pro-inflammatory activity and macrophage is present in early atherosclerotic lesions. The incidence of single nucleotide polymorphism (SNP) in the three major polymorphic region of NOD2 gene (SNP8, SNP12 and SNP13) was assessed in 182 RTR and the correlation between such polymorphism and the development of AE was analyzed. No correlation was observed between NOD2 gene polymorphism and the occurrence of AE after renal transplantation. NOD2 gene polymorphism thus does not appear to influence cardiovascular complications in RTR

    The Interleukin-6 Gene Promoter Polymorphism -174 and Atherosclerotic Events in Overweight Transplanted Patients

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    Chronic inflammation plays a pivotal role in atherosclerosis. We hypothesized that combining overweight and a greater genetic capacity to produce IL-6 predicted by IL-6 gene promoter polymorphism at position -174 (G→C) may allow to identify individuals exhibiting higher IL-6 and C-reactive protein (CRP) concentrations with a higher risk of atherosclerotic events (AE). The occurrence of AE was analyzed with respect to body mass index, IL-6 gene promoter polymorphism at position -174 (G→C), and other relevant risk factors, retrospectively, in 217 renal transplant recipients and, prospectively, in 132. Circulating IL-6 concentrations were closely related to BMI (r = 0.55, P = .0005). In overweight patients, serum IL-6 concentration was found to be significantly lower in C carriers than in GG patients (4.2 [1.0–5.1] versus 7.3 pg/mL [4.4–100]; P = .025). The incidence of AE was higher in overweight GG patients (29.5% versus 10.1%; P = .0003). In multivariate analysis, overweight-GG had an increased risk to develop AE (HR 2.96 [95% CI 1.09–8.04], P = .034 in the retrospective cohort, and HR 2.99 [95% CI 0.92–9.33], P = .069 in the prospective cohort). All these data are consistent with a role for both genetic and environmental determinants of inflammation (white adipose tissue mass) in the development of AE in renal transplanted patients

    [Physiopathology and treatment of nephrotic syndrome complications.]

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    International audienceThe nephrotic syndrome is defined by a urinary protein excretion exceeding 3g per day, associated with hypoalbuminaemia (<30g/L) and hypoprotidaemia (<60g/L). The clinical consequences of the nephrotic syndrome are multiple, essentially dominated by sodium retention and oedema formation. The oedema physiopathology is related to both increased capillary permeability and primary activation of the Na/K pump in the collect duct. Other complications of the nephrotic syndrome include thromboembolic complications, dyslipidaemia, and infections. The treatment of these complications represents an important part of the general management of the nephritic syndrome

    Aspects immunologiques de l'athérosclérose chez le transplanté rénal

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    BESANCON-BU MĂ©decine pharmacie (250562102) / SudocSudocFranceF

    Prevention of Post-Transplant Diabetes Mellitus: Towards a Personalized Approach

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    Post-transplant diabetes is a frequent complication after transplantation. Moreover, patients suffering from post-transplant diabetes have increased cardiovascular morbidity and reduced survival. Pathogenesis mainly involves beta-cell dysfunction in presence of insulin resistance. Both pre- and post-transplant risk factors are well-described, and some of them may be corrected or prevented. However, the frequency of post-transplant diabetes has not decreased in recent years. We realized a critical appraisal of preventive measures to reduce post-transplant diabetes

    Le polymorphisme (-174 G/C) du promoteur du gène de l'IL-6 influence la survenue d'un diabète de novo post-transplantation rénale

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    BESANCON-BU MĂ©decine pharmacie (250562102) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

    Ureteral stent placement and BK virus allograft nephropathy in renal transplant recipients.

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