Mechanisms of vascular calcification in uremia

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 × phosphate product (Ca × P), hyperphosphatemia may have direct effects on SMCs that predispose these cells to calcium deposition in end-stage renal disease patients.

Keywords:  vascular calcification , uremia , sodium-dependent phosphate cotransporter , biomineralization , hyperphosphatemia