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(Hypertension. 2006;47:1027.)
© 2006 American Heart Association, Inc.

Brief Review

Calcification and Cardiovascular Health

New Insights Into an Old Phenomenon

From the Department of Nephrology and Clinical Immunology (M.K., G.S.), University Hospital Aachen, and RWTH University Hospital Aachen (J.F.), Germany.

Correspondence to Markus Ketteler, Medizinische Klinik II: Nephrologie und klinische Immunologie, Universitätsklinikum Aachen, Pauwelsstr 30, D-52057 Aachen, Germany. E-mail mketteler@ukaachen.de

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

	Introduction

 
Uremic cardiovascular disease is characterized by accelerated calcifying atherosclerosis and valvular heart disease. Vascular calcification develops at 2 different sites within the vessel wall. Although intimal plaque calcification is a feature of genuine atherosclerosis, medial calcification is restricted to the smooth muscle cell layer and especially to the elastic laminae of arterial vessels (Figure 1). Both entities can be frequently observed in chronic kidney disease (CKD) patients. Dialysis patients with intimal calcifications are elderly and characterized by a history of "traditional" risk factors (eg, smoking and dyslipidemia) before the start of dialysis, whereas those with medial calcifications are, on average, 20 years younger and characterized by a longer time on dialysis treatment and a higher incidence of derangements in their calcium (Ca)xphosphate (P) balance.¹ Another recent study in incident dialysis patients showed that those with rapid arterial calcification progress already had calcified coronary arteries before reaching the dialysis stage.² This emphasizes that diagnostic, preventive, and therapeutic measures need to be initiated in early CKD stages. The clinical importance of this notion is stressed by a number of reports demonstrating that coronary artery and valvular calcifications occur prematurely and are very prevalent in dialysis patients and that they are independent risk factors of cardiovascular death in this patient group.^1,3–7 Such calcifications can, therefore, serve to at least partially explain why cardiovascular mortality is dramatically increased in the uremic as compared with a normal population and why it is not appropriately explained by the traditional Framingham risk factors.⁸ . . . [Full Text of this Article]

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