关键词: 血管钙化, 透析, 机制, 进展

Abstract: Vascular calcification is an active process of vascular smooth muscle cells (VSMC) trans-differentiating into osteoblast-like cells under precise control. Hyperphosphatemia induces VSMC trans-differentiating into osteoblast- like cells and up-regulation of fibroblast growth factor (FGF23), which together with Klotho is the pathogenic factor for vascular calcification. Higher serum FGF23 is associated with vascular calcification, but Klotho protein expression is significantly reduced in kidney tissues of chronic renal failure patients. In animal uremia models, supplement of recombinant osteoprotegerin (OPG) alleviates vascular calcification in mice with insufficient LDL receptors, and increase of the receptor activator of nuclear factor-kappa B ligand (RANKL) mediates the vascular calcification induced by angiotensin II. The effects of oxidative stress on vascular calcification may relate to the peroxide products and the lower resistance to oxidative stress. High turnover bone disease is the most common osteopathy in uremic patients. Higher serum parathyroid hormone (PTH) promotes bone reconstruction, osteoclast formation and bone re-absorption. The decrease of calcification inhibitors such as fetuin A and pyrophosphate in the serum of uremic patients also accelerates the vascular calcification.

Key words: Vascular calcification, Dialysis, Mechanism, Progression