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大动脉僵硬度作为脑腔隙性梗死与肾白蛋白尿之间的联系。

Large artery stiffening as a link between cerebral lacunar infarction and renal albuminuria.

作者信息

Hashimoto Junichiro, Aikawa Tomoyuki, Imai Yutaka

机构信息

Department of Planning for Drug Development and Clinical Evaluation, Tohoku University Graduate School of Pharmaceutical Science and Medicine, Sendai, Japan.

出版信息

Am J Hypertens. 2008 Dec;21(12):1304-9. doi: 10.1038/ajh.2008.291. Epub 2008 Sep 18.

DOI:10.1038/ajh.2008.291
PMID:18802428
Abstract

BACKGROUND

Stiffening of large arteries increases pulsatile pressure and flow stresses, which extend to the microcirculation in vasodilated organs such as the brain and kidneys. Subclinical cerebral lacunar infarction and albuminuria, both of which are early manifestations of microvascular damage, have been shown to be potentially interrelated in hypertension and with aging, but the underlying pathogenesis remains unknown.

METHODS

In a population of 351 general adults aged > or =50 years, urinary albumin/creatinine ratio (ACR), pulse wave velocity (PWV), and 24-h ambulatory blood pressure (BP) were measured, and cerebral lacunar lesions were assessed on magnetic resonance imaging (MRI).

RESULTS

Lacunar infarction was present in 86 subjects (25%). Subjects with lacunae had a higher median urinary ACR than those without (20.6 vs. 14.6 mg/g.Cr, P = 0.004). The positive association between the presence of lacunae and urinary ACR remained significant in a logistic model that adjusted for covariates including age, gender, and 24-h BP (P = 0.04); the odds ratio (OR) for lacunae was 1.32 for each 1 s.d. increase in urinary ACR. However, when PWV was added to this model, increased PWV but not urinary ACR was associated with lacunae. There was a significant interaction between urinary ACR and PWV with respect to lacunae; only subjects with a high PWV above the median showed an independent association between urinary ACR and the presence of lacunae (P = 0.03).

CONCLUSIONS

Microvascular damage in the brain (lacunar infarction) and kidney (albuminuria) appears to be interrelated in the general population. Large arterial stiffening may play a pivotal role in this cerebro-renal connection.

摘要

背景

大动脉僵硬度增加会使搏动压力和血流应力增大,进而延伸至脑和肾等血管扩张器官的微循环。亚临床脑腔隙性梗死和蛋白尿均为微血管损伤的早期表现,已证实在高血压及衰老过程中二者可能存在关联,但其潜在发病机制仍不明。

方法

在351名年龄≥50岁的普通成年人中,测量尿白蛋白/肌酐比值(ACR)、脉搏波速度(PWV)及24小时动态血压(BP),并通过磁共振成像(MRI)评估脑腔隙性病变。

结果

86名受试者(25%)存在腔隙性梗死。有腔隙的受试者尿ACR中位数高于无腔隙者(20.6对14.6mg/g.Cr,P = 0.004)。在调整了年龄、性别和24小时BP等协变量的逻辑模型中,腔隙的存在与尿ACR之间的正相关仍然显著(P = 0.0​​4);尿ACR每增加1个标准差,腔隙的优势比(OR)为1.32。然而,当将PWV添加到该模型中时,与腔隙相关的是PWV升高而非尿ACR。在腔隙方面,尿ACR与PWV之间存在显著交互作用;仅PWV高于中位数的高PWV受试者中,尿ACR与腔隙的存在之间显示出独立关联(P = 0.03)。

结论

在普通人群中,脑(腔隙性梗死)和肾(蛋白尿)的微血管损伤似乎相互关联。大动脉僵硬度增加可能在这种脑肾联系中起关键作用。

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