Cozzolino M, Gallieni M, Brancaccio D
Renal Division, S. Paolo Hospital, University of Milan, Milan, Italy.
Int J Artif Organs. 2008 Dec;31(12):1002-3. doi: 10.1177/039139880803101203.
Extensive calcification of the arterial wall and soft tissues is a frequent feature of patients with end-stage chronic kidney disease (CKD stage 5). Hyperphosphatemia and secondary hyperparathyroidism have been extensively investigated as inducing factors in cardiovascular calcification. In fact, cardiovascular disease in renal failure is associated with bone metabolism alterations. Together with passive deposition of calcium-phosphate in extraskeletal tissues, it has recently been demonstrated that inorganic phosphate induces arterial calcification directly through a real "ossification" of the tunica media in the vasculature of CKD patients. Therefore, control of serum phosphate in CKD patients becomes crucial in preventing increases in calcium x phosphate product, secondary hyperparathyroidism, and ultimately vascular calcification.
动脉壁和软组织广泛钙化是终末期慢性肾脏病（CKD 5期）患者的常见特征。高磷血症和继发性甲状旁腺功能亢进作为心血管钙化的诱导因素已得到广泛研究。事实上，肾衰竭患者的心血管疾病与骨代谢改变有关。除了钙磷在骨骼外组织中的被动沉积外，最近还证明无机磷通过CKD患者血管中中膜的真正“骨化”直接诱导动脉钙化。因此，控制CKD患者的血清磷对于预防钙磷乘积增加、继发性甲状旁腺功能亢进以及最终的血管钙化至关重要。
