多灶性纤维肌发育不良与动脉粥样硬化性肾动脉狭窄之间的病理生理差异。

Pathophysiological differences between multifocal fibromuscular dysplasia and atherosclerotic renal artery stenosis.

作者信息

van Twist Daan J L, Houben Alfons J H M, de Haan Michiel W, de Leeuw Peter W, Kroon Abraham A

机构信息

aDepartment of Internal Medicine bCardiovascular Research Institute Maastricht (CARIM) cDepartment of Radiology, Maastricht University Medical Center (MUMC+), Maastricht dDepartment of Internal Medicine, Zuyderland Medical Center, Sittard, The Netherlands.

出版信息

J Hypertens. 2017 Apr;35(4):845-852. doi: 10.1097/HJH.0000000000001243.

DOI:10.1097/HJH.0000000000001243

PMID:28060190

Abstract

BACKGROUND

Fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS) are the most common causes of renovascular hypertension. So far, FMD is believed to cause hypertension via similar mechanisms as in ARAS, that is, a decrease in renal blood flow, which subsequently leads to increased renin secretion. However, given the differences in the blood pressure (BP)-lowering effect of revascularization between patients with ARAS and FMD, we questioned whether this is true.

METHODS

We measured renal blood flow (Xenon washout method) and renin secretion per kidney and their relationship to BP in a cohort of 64 patients with multifocal FMD and 110 patients with ARAS (off medication, prior to revascularization).

RESULTS

We found that renal blood flow is significantly higher in FMD as compared with ARAS. In patients with unilateral ARAS, renin secretion was increased in the affected kidney as compared with the unaffected kidney. This lateralization in renin secretion, however, was not found in unilateral FMD. After correction for differences in baseline characteristics, we found that systemic renin levels and local renin secretion was lower in FMD as compared with ARAS. Moreover, the relationship between BP and renin secretion in FMD was inverse to that in ARAS.

CONCLUSION

These findings argue against the hypothesis that FMD induces hypertension via similar pathophysiological mechanism as in ARAS.

摘要

背景

纤维肌性发育不良（FMD）和动脉粥样硬化性肾动脉狭窄（ARAS）是肾血管性高血压最常见的病因。迄今为止，人们认为FMD通过与ARAS类似的机制导致高血压，即肾血流量减少，继而导致肾素分泌增加。然而，鉴于ARAS和FMD患者血管重建后血压降低效果存在差异，我们质疑这是否属实。

方法

我们采用氙清除法测量了64例多灶性FMD患者和110例ARAS患者（未服药，血管重建术前）的肾血流量、单肾肾素分泌情况及其与血压的关系。

结果

我们发现，与ARAS相比，FMD患者的肾血流量显著更高。在单侧ARAS患者中，患侧肾脏的肾素分泌较未受影响的肾脏增加。然而，单侧FMD患者未发现肾素分泌的这种侧化现象。校正基线特征差异后，我们发现，与ARAS相比，FMD患者的全身肾素水平和局部肾素分泌更低。此外，FMD患者血压与肾素分泌之间的关系与ARAS患者相反。