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JASN:肾脏衰竭或增加心脏疾病发病风险

2013-05-06 T.Shen 生物谷

肾衰竭个体通常会引发心脏问题,但是具体原因并不清楚,近日,刊登在国际杂志Journal of the American Society of Nephrology上的一项研究提出了相关线索,文章中,研究者表示,肾脏将废弃物分泌到尿液的功能的缺失会使得这些废弃物进入血液,这或许会影响患者血管内壁的含糖量以及导致心脏疾病发生。 来自阿姆斯特丹的学术医疗中心的研究者想知道,是否包被血管内部的一个血糖层

肾衰竭个体通常会引发心脏问题,但是具体原因并不清楚,近日,刊登在国际杂志Journal of the American Society of Nephrology上的一项研究提出了相关线索,文章中,研究者表示,肾脏将废弃物分泌到尿液的功能的缺失会使得这些废弃物进入血液,这或许会影响患者血管内壁的含糖量以及导致心脏疾病发生。

来自阿姆斯特丹的学术医疗中心的研究者想知道,是否包被血管内部的一个血糖层-糖萼(glycocalyx),在肾衰竭病人中受到了损伤,而且是增加心脏问题风险的主要原因?因此研究者开展了此项研究,他们使用了一种新型的成像技术来监测40个病人和21个健康个体的血管,同时也测定了病人血管中的糖萼组分。

相比健康个体,肾衰竭病人血管中失去了部分的糖萼层,而且其血液中的糖萼组分水平过高,这也就表明患者血管中糖萼层的脱落发生了增加。

研究者Vlahu表示,损伤的糖萼屏障和其组分进入血液中,很有可能引发患者严重的血管中病理学表现。内皮糖萼的状态及其循环组分可以为检测血管易损伤性、检测早期疾病以及评价疾病风险提供一定的研究工具

肾脏衰竭相关的拓展阅读:

Damage of the Endothelial Glycocalyx in Dialysis Patients

Damage to the endothelial glycocalyx, which helps maintain vascular homeostasis, heightens the sensitivity of the vasculature to atherogenic stimuli. Patients with renal failure have endothelial dysfunction and increased risk for cardiovascular morbidity and mortality, but the state of the endothelial glycocalyx in these patients is unknown. Here, we used Sidestream Darkfield imaging to detect changes in glycocalyx dimension in dialysis patients and healthy controls from in vivo recordings of the sublingual microcirculation. Dialysis patients had increased perfused boundary region and perfused diameters, consistent with deeper penetration of erythrocytes into glycocalyx, indicating a loss of glycocalyx barrier properties. These patients also had higher serum levels of the glycocalyx constituents hyaluronan and syndecan-1 and increased hyaluronidase activity, suggesting the shedding of these components. Loss of residual renal function had no influence on the imaging parameters but did associate with greater shedding of hyaluronan in blood. Furthermore, patients with higher levels of inflammation had more significant damage to the glycocalyx barrier. In conclusion, these data suggest that dialysis patients have an impaired glycocalyx barrier and shed its constituents into blood, likely contributing to the sustained endothelial cell activation observed in ESRD.

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