Abstract
Cardiovascular disease is the first cause of morbidity and mortality in dialysis patients. Hyperphosphatemia and elevated serum calcium-phosphate levels have recently been investigated as inducing factors on extraskeletal calcification in this population. In vitro studies demonstrated that human aortic smooth muscle cells calcify when incubated in a high phosphate medium, where calcium and calcitriol are not changed. Furthermore, the lack of inhibitory proteins, such as fetuin and matrix Gla protein, is a possible main determinant of calcium-phosphate deposition in soft tissues. The classical treatment of hyperphosphatemia and secondary hyperparathyroidism in dialysis patients consists of calcium-based phosphate binders and calcitriol administration. Unfortunately, this "first-generation" therapy is not free of dramatic side effects. New free-calcium and -aluminum phosphate binders, new vitamin D metabolites, and calcimimetics are examples of "second-generation" therapies that may prevent vascular calcification and possibly prevent some of the burden of cardiovascular disease in uremia.
Translated title of the contribution | Cardiovascular calcification and atherosclerosis accelerated during uremia |
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Original language | Italian |
Pages (from-to) | 25-28 |
Number of pages | 4 |
Journal | Italian Heart Journal Supplement |
Volume | 6 |
Issue number | 1 |
Publication status | Published - Jan 2005 |
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine