Background: Vascular calcification is believed to have a crucial role in the excess cardiovascular mortality and morbidity in patients with end-stage renal disease (ESRD).
Methods and results: Recent evidence suggests that uremic vascular calcification is an active cell-mediated process resembling osteogenesis in bone, rather than passive precipitation of calcium and phosphorus in the setting of deranged mineral metabolism. To date, several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, and type I collagen) have been shown in histological sections of vessels obtained from patients with ESRD or calcific uremic arteriolopathy. In in vitro experiments, the addition of uremic serum upregulates osteopontin expression by cultured vascular smooth muscle cells (VSMCs).
Conclusion: We are only beginning to understand the process by which VSMCs transform into osteoblast-like cells, although phosphorus may have a key role. Additional factors mediating or modulating the development of vascular calcification in patients with ESRD remain to be identified. Further understanding of the pathophysiological state of uremic vascular calcification is needed to design effective therapeutic strategies to intervene with this devastating condition in the ESRD population.