中国血液净化

中国血液净化 ›› 2017, Vol. 16 ›› Issue (03): 183-187.doi: 10.3969/j.issn.1671-4091.2017.03.010

• 基础研究 • 上一篇    下一篇

动静脉内瘘成形术前静脉内膜增生机制的探讨

范晶娴1,庄峰1,卢建新1,王应灯1   

  1. 1. 上海交通大学 医学院附属第九人民医院肾脏科
  • 收稿日期:2016-06-17 修回日期:2017-01-17 出版日期:2017-03-12 发布日期:2017-03-12
  • 通讯作者: 王应灯 wangyd7001@sina.com E-mail:WangYd7001@sina.com

The mechanism of venous neointimal hyperplasis before the AVF operation in ESRD patients

  • Received:2016-06-17 Revised:2017-01-17 Online:2017-03-12 Published:2017-03-12

PDF

449

摘要： 目的近期研究发现终末期肾脏病(end-stage renal disease，ESRD)患者于动静脉内瘘(arteriovenous fistula，AVF)成形术前就已经发生不同程度的静脉内膜增生，本研究对此进行相关机制的探讨。方法分别筛选出首次进行AVF 成形术静脉增生内膜8 例(简称AVF 成形术组)，需要进行AVF 修补术静脉增生内膜8 例(简称AVF 修补术组)，2 组分别进行免疫组织学研究，主要包括平滑肌肌动蛋白(smooth muscle actin,SMA)、波形蛋白(Vimentin)、结蛋白(Desmin)以及I 型血小板结合蛋白基序的解聚蛋白样金属蛋白酶(a disintegrin- like and metalloproteinase with thrombospondin type l motifs-1, ADAMTS-1)。结果AVF 成形术组的增生内膜层出现平滑肌细胞浸润，大部分表型为SMA+、Vimentin+、Desmin-的成肌纤维平滑肌细胞(myofibroblasts)，少部分表现为SMA+、Desmin+、Vimentin-的收缩型平滑肌细胞(contractile smooth muscle cells)；而AVF 修补术组的增生内膜中，几乎所有的平滑肌细胞表型均为SMA+、Vimentin+、Desmin-的成肌纤维平滑肌细胞。AVF 成形术组中ADAMTS-1 表达均阴性，AVF 修补术组仅1 例出现ADAMTS-1 阳性表达。结论成肌纤维平滑肌细胞是参与AVF 术前静脉内膜增生的重要角色，阻断该平滑肌细胞表型的转化及迁移可能是治疗内膜增生的一个有效方法。

关键词: 终末期肾病, 动静脉内瘘狭窄, 内膜增生, 平滑肌细胞表型

Abstract: Objective Recently, some researchers found that venous neointimal hyperplasis existed before AVF operation in ESRD patients. We explored the mechanism of the venous neointimal hyperplasis. Methods We screened out 8 patients with venous neointimal hyperplasis during the first AVF operation (the AVF operation group), and 8 patients with venous neointimal hyperplasis during ateriovenous fistula repair operation (the AVF repair group). Venous samples were subjected to immunohistochemistry for the expression of smooth muscle actin (SMA), vimentin, desmin and a disintegrin-like and metalloproteinase with thrombospondin
type l motifs-1 (ADAMTS1) to explore the mechanism of venous neointimal hyperplasis. Result In the AVF operation group, most cells in the hyperplastic neointima layer were myofibroblasts with SMA+, vimentin+ and desmin-, and a few cells were contractile smooth cells with SMA+, vimentin- and desmin+. In the
AVF repair group, almost all cells in the hyperplastic neointima layer were myofibroblasts with SMA+, vimentin+, and desmin-. ADAMTS1 staining was negative in the AVF operation group and was positive in one venous sample in the AVF repair group. Conclusion Myofibroblasts play an important role in the neointimal
hyperplasis before AVF operation in ESRD patients. Blocking the phenotypic transformation and migration of smooth muscle cells may be an effective way to cure the neointimal hyperplasis.

Key words: ESRD, arteriovenous fistula stenosis, neointimal hyperplasis, smooth muscle phenotype