Coen G, Manni M, Mantella D, Splendiani G
Nefrologia ed Ipertensione, Ospedale Israelitico, Rome.
G Ital Nefrol. 2006 Jan-Feb;23 Suppl 34:S21-5.
Chronic kidney disease, with special regard to hemodialysis patients, develop frequent and widespread cardiac and vascular calcifications. In the heart calcifications are mainly located in the coronary arteries and in the valvular structures. There is a strict relation between cardiovascular mortality in CKD and the extent of cardiac and vascular calcifications. Therefore it is important to evaluate the causes of extraskeletal calcifications for the evaluation of the possibility of prevention. The importance of hyperphosphatemia, of hypercalcemia and of the increased CAxP product as a cause of cardiac calcification has been clearly underlined. However the mechanism of calcification, initially considered a physico-chemical precipitation, has been investigated with the conclusion that the process is mediated by cellular differentiation and production of factors favoring mineralization in the extracellular milieu. Increased serum phosphate levels are able to induce a transformation of vascular smooth muscle cells into osteoblast-like cells, able to produce factors known to be pro-mineralizing agents in the bone tissue. Further studies have revealed the importance of a number of inhibitors of calcification of cardiovascular structures, like Fetuin-A, MGP, Osteopontin, Osteoprotegerin. Therefore at present the calcification process of vascular tissue is considered to be linked to a balance between inducers and inhibitors of calcium-phosphate deposits. Prevention of cardiac calcifications is at present mainly based of optimal control of serum phosphate and reduction of calcium load through the use of non-calcium containing phosphate binders. Treatment with statins for prevention and treatment of atherosclerosis is also an important means of decreasing the size and number of atherosclerotic plaques, where a portion of the calcification process develops.
慢性肾脏病，尤其是血液透析患者，常出现广泛的心脏和血管钙化。在心脏中，钙化主要位于冠状动脉和瓣膜结构。慢性肾脏病患者的心血管死亡率与心脏和血管钙化程度密切相关。因此，评估骨外钙化的原因对于评估预防的可能性很重要。高磷血症、高钙血症以及钙磷乘积增加作为心脏钙化原因的重要性已得到明确强调。然而，钙化机制最初被认为是一种物理化学沉淀，经过研究得出结论，该过程是由细胞分化和细胞外环境中促进矿化的因子产生介导的。血清磷酸盐水平升高能够诱导血管平滑肌细胞转化为成骨样细胞，这些细胞能够产生已知在骨组织中是促矿化剂的因子。进一步的研究揭示了一些心血管结构钙化抑制剂的重要性，如胎球蛋白-A、基质Gla蛋白、骨桥蛋白、骨保护素。因此，目前血管组织的钙化过程被认为与钙磷沉积的诱导剂和抑制剂之间的平衡有关。目前预防心脏钙化主要基于对血清磷酸盐的最佳控制以及通过使用不含钙的磷结合剂减少钙负荷。使用他汀类药物预防和治疗动脉粥样硬化也是减少动脉粥样硬化斑块大小和数量的重要手段，钙化过程部分发生在这些斑块中。
