神经药理学报

神经药理学报 ›› 2026, Vol. 16 ›› Issue (3): 60-.DOI: 10.3969/j.issn.2095-1396.2026.03.009

• 综述 • 上一篇    

血压变异性联合胱抑素C水平与血管性认知障碍的研究进展

吕晓朔，魏嘉宁，薛茜，邹玉安   

  1. 1. 河北北方学院研究生学院，张家口，075000，中国 

    2. 河北北方学院附属第一医院神经内科，张家口，075000，中国

  • 出版日期:2026-06-26 发布日期:2026-08-05
  • 通讯作者: 薛茜，主任医师，教授，硕士生导师；研究方向：神经内科疾病
  • 作者简介:吕晓朔，2024 级硕士研究生；研究方向：神经病学

Research Progress on the Association Between Blood Pressure Variability and Cystatin C Levels in Vascular Cognitive Impairment

LV Xiao-shuo, WEI Jia-ning, XUE Qian, ZOU Yu-an   

  1. 1. Graduate School, Hebei North University, Zhangjiakou, 075000, China 

    2. Department of Neurology, the First Affiliated Hospital of Hebei North University, Zhangjiakou, 075000, China

  • Online:2026-06-26 Published:2026-08-05

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摘要：

血管性认知障碍（vascular cognitive impairment， VCI）已成为当今老龄化社会面临的重要健康挑战，其 核心病理基础在于脑血管的病变。而血压变异性（blood pressure variability， BPV）作为反映血压动态波动的指 标，与肾功能敏感标志物胱抑素 C（cystatin C， Cys-C）水平，均被证实与 VCI 密切相关。研究表明，增大的 BPV 通过损害肾脏血管内皮细胞功能，引发肾脏亚临床损伤与微血管病变，进而导致 Cys-C 水平升高，升高的 Cys-C 不仅反映了肾损伤，其本身也可能参与系统性血管炎症与动脉硬化。最终，这种由 BPV 启动、经肾脏血管内皮功 能障碍与 Cys-C 水平变化所表征的“肾源性”损害，通过加剧脑小血管病（cerebral small vessel disease，CSVD）、 神经炎症等多种途径，共同推动了 VCI 的发生与发展。该文从这一连锁机制的研究进展进行综述，并探讨了联 合评估 BPV 与 Cys-C 水平在 VCI 早期识别中的潜在价值。

关键词: 血压变异性, 胱抑素 C, 血管性认知障碍, 肾脏, 内皮功能障碍

Abstract:

To Vascular cognitive impairment (VCI) has emerged as a significant health challenge in today's aging societies, with its core pathological basis rooted in cerebral vascular lesions. Blood pressure variability (BPV), an indicator reflecting dynamic blood pressure fluctuations, and cystatin C (Cys-C) levels—a sensitive marker of renal function—have both been demonstrated to be closely associated with VCI. Research indicates that increased BPV impairs renal vascular endothelial cell function, triggering subclinical renal injury and microvascular pathology. This, in turn, elevates Cys-C levels. Elevated Cys-C not only reflects renal damage but may also contribute to systemic vascular inflammation and atherosclerosis. Ultimately, this “renal-originating” damage—initiated by BPV and characterized by renal vascular endothelial dysfunction and altered Cys-C levels—contributes to the onset and progression of VCI through multiple pathways, including exacerbating cerebral small vessel disease (CSVD) andneuroinflammation. This review summarizes research progress on this chain mechanism and explores the potential value of jointly assessing BPV and Cys-C levels for early identification of VCI.

Key words: blood pressure variability, cystatin C, vascular cognitive impairment, kidney, endothelial dysfunction

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