12 research outputs found

    VITA-D: Cholecalciferol substitution in vitamin D deficient kidney transplant recipients: A randomized, placebo-controlled study to evaluate the post-transplant outcome

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Vitamin D does not only regulate calcium homeostasis but also plays an important role as an immune modulator. It influences the immune system through the induction of immune shifts and regulatory cells resulting in immunologic tolerance. As such, vitamin D is thought to exert beneficial effects within the transplant setting, especially in kidney transplant recipients, considering the high prevalence of vitamin D deficiency in kidney transplant recipients.</p> <p>Methods/Design</p> <p>The VITA-D study, a randomized, placebo-controlled, double-blind study with two parallel groups including a total of 200 kidney transplant recipients, is designed to investigate the immunomodulatory and renoprotective effects of cholecalciferol (vitamin D<sub>3</sub>) within the transplant setting. Kidney transplant recipients found to have vitamin D deficiency defined as 25-hydroxyvitamin D<sub>3 </sub>< 50 nmol per liter will be randomly assigned to receive either oral cholecalciferol therapy or placebo and will be followed for one year. Cholecalciferol will be administered at a dose of 6800 International Units daily over a time period of one year.</p> <p>The objective is to evaluate the influence of vitamin D<sub>3 </sub>substitution in vitamin D deficient kidney transplant recipients on the post-transplant outcome. As a primary endpoint glomerular filtration rate calculated with the MDRD formula (modification of diet in renal disease) one year after kidney transplantation will be evaluated. Incidence of acute rejection episodes, and the number and severity of infections (analyzed by means of C-reactive protein) within the first year after transplantation will be monitored as well. As a secondary endpoint the influence of vitamin D<sub>3 </sub>on bone mineral density within the first year post-transplant will be assessed. Three DXA analyses will be performed, one within the first four weeks post-transplant, one five months and one twelve months after kidney transplantation.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov NCT00752401</p

    Vitamine D et rein

    Full text link
    Le calcitriol et ses analogues inhibent le système rénineangiotensine- aldostérone, qui joue un rôle important dans le développement des lésions glomérulaires et tubulo-interstitielles et dans l’apparition de la protéinurie, mais aussi l’activation de la voie NF-kB qui est connue pour favoriser la maladie rénale chronique en stimulant l’inflammation et la fibrogenèse. Les effets pléiotropes de la vitamine D sont également très intéressants pour le patient insuffisant rénal (diminution de la mortalité, de la protéinurie et effets anti-inflammatoires). De plus, l’administration de vitamine D native (cholécalciférol ou ergocalciférol) diminue les concentrations sériques de parathormone. La supplémentation en vitamine D native chez l’insuffisant rénal n’entraîne pas de toxicité ni d’augmentation du risque de calcification vasculaire malgré les effets hypercalcémiants et hyperphosphorémiants de cette molécule sous sa forme active. La vitamine D per se (c’est-à-dire sans apports calciques excessifs), aux doses habituellement utilisées en clinique, n’est pas associée à une augmentation du risque de lithiase urinaire. Dans le domaine de la transplantation rénale, les études expérimentales montrent un rôle protecteur des analogues de la vitamine D contre le rejet aigu, mais les études cliniques restent à ce jour principalement observationnelles

    Tertiary excess of fibroblast growth factor 23 and hypophosphatemia following kidney transplantation

    No full text
    Hypophosphatemia due to inappropriate urinary phosphate wasting is a frequent metabolic complication of the early period following kidney transplantation. Although previously considered to be caused by tertiary hyperparathyroidism, recent evidence suggests a primary role for persistently elevated circulating levels of the phosphorus-regulating hormone, fibroblast growth factors 23 (FGF23). In the setting of a healthy renal allograft, markedly increased FGF23 levels from the dialysis period induce renal phosphate wasting and inhibition of calcitriol production, which contribute to hypophosphatemia. While such tertiary FGF23 excess and resultant hypophosphatemia typically abates within the first few weeks to months post-transplant, some recipients manifest persistent renal phosphate wasting. Furthermore, increased FGF23 levels have been associated with increased risk of kidney disease progression, cardiovascular disease and death outside of the transplant setting. Whether tertiary FGF23 excess is associated with adverse transplant outcomes is unknown. In this article, we review the physiology of FGF23, summarize its relationship with hypophosphatemia after kidney transplantation, and speculate on its potential impact on long term outcomes of renal allograft recipients
    corecore