Abstract
Vascular calcification and cardiovascular disease mortality are highly correlated with increased serum phosphate levels in end-stage renal disease patients. Mechanistic studies in cultured human smooth muscle cells (SMCs) indicate that increased phosphate levels induces both calcification and phenotypic transition through a pathway requiring a sodium-dependent phosphate cotransporter. Thus, in addition to contributing to increased calcium x phosphate product (Ca x P), hyperphosphatemia may have direct effects on SMCs that predispose these cells to calcium deposition in end-stage renal disease patients.
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