Effect of oral calcium carbonate on aortic calcification in apolipoprotein E-deficient (apoE-/-) mice with chronic renal failure.

Détails

Ressource 1Télécharger: serval:BIB_5FFFEBDED469.P001 (367.44 [Ko])
Etat: Public
Version: de l'auteur
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ID Serval
serval:BIB_5FFFEBDED469
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Effect of oral calcium carbonate on aortic calcification in apolipoprotein E-deficient (apoE-/-) mice with chronic renal failure.
Périodique
Nephrology, Dialysis, Transplantation
Auteur(s)
Phan O., Ivanovski O., Nikolov I.G., Joki N., Maizel J., Louvet L., Chasseraud M., Nguyen-Khoa T., Lacour B., Drüeke T.B., Massy Z.A.
ISSN
0931-0509
Statut éditorial
Publié
Date de publication
2008
Volume
23
Numéro
1
Pages
82-90
Langue
anglais
Résumé
BACKGROUND: In chronic kidney disease (CKD) patients, the intake of calcium-based phosphate binders is associated with a marked progression of coronary artery and aortic calcification, in contrast to patients receiving calcium-free phosphate binders. The aim of this study was to reexamine the role of calcium carbonate in vascular calcification and to analyse its effect on aortic calcification-related gene expression in chronic renal failure (CRF). METHODS: Mice deficient in apolipoprotein E underwent either sham operation or subtotal nephrectomy to create CRF. They were then randomly assigned to one of the three following groups: a control non-CRF group and a CRF group fed on standard diet, and a CRF group fed on calcium carbonate enriched diet, for a period of 8 weeks. Aortic atherosclerotic plaque and calcification were evaluated using quantitative morphologic image processing. Aortic gene and protein expression was examined using immunohistochemistry and Q-PCR methods. RESULTS: Calcium carbonate supplementation was effective in decreasing serum phosphorus but was associated with a higher serum calcium concentration. Compared with standard diet, calcium carbonate enriched diet unexpectedly induced a significant decrease of both plaque (p<0.05) and non-plaque-associated calcification surface (p<0.05) in CRF mice. It also increased osteopontin (OPN) protein expression in atherosclerotic lesion areas of aortic root. There was also a numerical increase in OPN and osteoprotegerin gene expression in total thoracic aorta but the difference did not reach the level of significance. Finally, calcium carbonate did not change the severity of atherosclerotic lesions. CONCLUSION: In this experimental model of CRF, calcium carbonate supplementation did not accelerate but instead decreased vascular calcification. If our observation can be extrapolated to humans, it appears to question the contention that calcium carbonate supplementation, at least when given in moderate amounts, necessarily enhances vascular calcification. It is also compatible with the hypothesis of a preponderant role of phosphorus over that of calcium in promoting vascular calcification in CRF.
Mots-clé
Administration, Oral, Animals, Aortic Diseases/chemically induced, Aortic Diseases/pathology, Apolipoproteins E/deficiency, Calcinosis/chemically induced, Calcinosis/pathology, Calcium Carbonate/administration & dosage, Calcium Carbonate/adverse effects, Female, Kidney Failure, Chronic/complications, Mice
Pubmed
Web of science
Open Access
Oui
Création de la notice
13/10/2009 11:41
Dernière modification de la notice
25/09/2019 7:09
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