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(Circulation Research. 2006;98:857.)
© 2006 American Heart Association, Inc.

Editorials

Pitting Phosphate Transport Inhibitors Against Vascular Calcification

Linda L. Demer, Yin Tintut

From the Departments of Medicine, Physiology, and Biomedical Engineering, The David Geffen School of Medicine at UCLA.

Correspondence to Linda L. Demer, MD, PhD, Department of Medicine, BH-307 Center for Health Sciences, 10833 LeConte Avenue, Los Angeles, CA 90095-1679. E-mail Ldemer@mednet.ucla.edu

See related article, pages 905–912

Key Words: vascular • calcification • Pit-1 • mineralization • phosphate transport

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Vascular calcification is widespread in patients with coronary artery disease, peripheral vascular disease, and diabetes, but by far the most severe and extensive vascular calcification is in those with end-stage renal disease, especially those with the longest exposure to hemodialysis. Their coronary calcification scores on electron beam CT scanning are often an order of magnitude greater than in ordinary CAD patients. The severity of their vascular calcification closely relates to the duration of hemodialysis; after a decade of dialysis, even pediatric patients are affected.¹ Histopathologically, these calcium deposits are located primarily in the medial layer, unlike atherosclerotic calcification, which is located within the intimal lesions. This and other differences suggest that the two forms may have different underlying mechanisms. Although it remains controversial whether vascular calcification promotes plaque destabilization, it is clear that arterial rigidity contributes to hypertension, cardiac hypertrophy, and heart failure, in part because of increased aortic impedance, as seen in experimental models that use aortic banding to produce heart failure. This is likely the reason that patients with chronic renal disease most often die of cardiovascular complications.

This clinical phenomenon offers important mechanistic clues about vascular calcification, as recognized by Giachelli and colleagues at University of Washington. As a result of their interdisciplinary work, they were aware that bone biologists routinely treat their osteoblast cultures with phosphate supplements, usually in the form of beta-glycerophosphate, and that phosphate supplements accelerated osteoblast mineralization. Together with the knowledge that end-stage renal disease patients almost uniformly have both elevated serum phosphate . . . [Full Text of this Article]

Related Article:

Role of the Sodium-Dependent Phosphate Cotransporter, Pit-1, in Vascular Smooth Muscle Cell Calcification

Xianwu Li, Hsueh-Ying Yang, and Cecilia M. Giachelli
Circ. Res. 2006 98: 905-912. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				W. C. O'Neill Pyrophosphate, Alkaline Phosphatase, and Vascular Calcification Circ. Res., July 21, 2006; 99(2): e2 - e2. [Full Text] [PDF]