慢性肾脏病患者继发性甲状旁腺功能亢进与心血管钙化的联系及意义  

Relationship between secondary hyperparathyroidism and cardiovascular calcification in chronic kidney disease patients and its clinical implication

作　　者：林珊[1] 贾俊亚[1] 

机构地区：[1]天津医科大学总医院肾内科,300052

出　　处：《中华肾病研究电子杂志》2013年第2期21-24,共4页Chinese Journal of Kidney Disease Investigation（Electronic Edition）

基　　金：国家自然科学基金资助项目(81270791);天津市卫生局重点攻关课题(11KG132);天津市应用基础及前沿计划(10JCYBC11700)

摘　　要：继发性甲状旁腺功能亢进(SHPT)与心血管钙化是慢性肾脏病(CKD)患者常见临床表现,二者常伴随出现,密切相关。SHPT可通过对钙磷代谢的影响而间接导致或加重心血管钙化,但它对心血管钙化的直接影响尚未明确。研究表明,生理剂量的甲状旁腺素(PTH)对血管平滑肌细胞(VSMC)增殖及钙化有抑制作用,而超生理剂量PTH则有促进作用,后者可能通过增加炎症介质或促进钙化基因的转录而实现。因此,防治SHPT是干预心血管钙化的重要手段。甲状旁腺切除术、限制饮食磷摄入、使用磷结合剂、活性维生素D及其类似物等措施可有效改善SHPT,但它们对血管钙化的影响尚无明确结论。最近发现,西那卡塞可延缓透析患者心血管钙化的进展,这为药物干预SHPT同时防治心血管钙化提供了重要依据。Secondary hyperparathyroidism （SHPT） is often accompanied by cardiovascular calcification in chronic kidney disease （CKD） patients. Through its effects on calcium and phosphorus metabolism, SHPT can indirectly cause or aggravate vascular calcification. However, the direct effects of parathyroid hormone （PTH） on cardiovascular calcification are biphasic. Physiological dose of PTH inhibits vascular smooth musclecells （VSMC） proliferation and calcification while supraphysiological dose of PTH promotes these processes by increasing inflammatory mediators such as IL-6, RAGE or by promoting transcription of the calcification gene. Therefore, prevention of SHPT is important for intervention in the cardiovascular calcification. It has been found that parathyroidectomy, dietary phosphorus restriction, use of phosphate binders, active vitamin D and/or its analogs may effectively improve SHPT, but their effects on vascular calcification still remains unclear yet. Recently, cinacalcet, the only drug of calcimimetics, has been found to slow down the progression of cardiovascular calcification in dialysis patients, which provides important evidence for prevention of the cardiovascular calcification with anti-SHPT drugs in CKD patients.

关 键 词：继发性甲状旁腺功能亢进 钙化 心血管 甲状旁腺激素 

分 类 号：R692.5[医药卫生—泌尿科学]