Qunibi Wajeh Y, Nolan Charles A, Ayus J Carlos
Division of Nephrology, Department of Medicine, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, USA.
Kidney Int Suppl. 2002 Dec(82):S73-80. doi: 10.1046/j.1523-1755.62.s82.15.x.
The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.
终末期肾病（ESRD）患者心血管疾病的死亡风险增加。这是由传统因素和透析特有的因素共同导致的。最近，一些透析特有的风险因素被认为与心血管钙化的发病机制有关。这些因素包括：高磷血症、高钙磷（Ca×P）乘积、甲状旁腺激素水平升高、透析时间、含钙磷结合剂和维生素D类似物的治疗。电子束计算机断层扫描（EBCT）的出现，使人们对ESRD患者心血管钙化的发生有了更高的认识。鉴于使用含钙结合剂会出现短暂高钙血症，有人提出使用含钙磷结合剂导致的钙负荷与冠状动脉钙化的发生之间存在联系。然而，这些药物的使用与心血管钙化之间的因果关系尚未确立。此外，早在这些磷结合剂出现之前的一个多世纪，人们就已经认识到了这种现象。尽管其发病机制可能是多因素的，但现有数据强烈表明血清磷升高是主要原因。此外，维生素D治疗可能会加重钙化风险，尤其是在严重继发性甲状旁腺功能亢进的患者中。因此，严格控制血清磷、Ca×P乘积和甲状旁腺激素水平可能会减少心血管钙化，并提高维持性血液透析患者的生存率。由于醋酸钙是最具成本效益的磷结合剂，我们建议它应仍然是ESRD患者高磷血症的一线治疗药物。
