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低三碘甲状腺原氨酸可改变晚期非糖尿病肾病患者的血流介导的血管舒张功能。

Low triiodothyronine alters flow-mediated vasodilatation in advanced nondiabetic kidney disease.

机构信息

Department of Nephrology, Gülhane School of Medicine, Ankara, Turkey.

出版信息

Am J Nephrol. 2011;33(1):25-32. doi: 10.1159/000322581. Epub 2010 Dec 9.

DOI:10.1159/000322581
PMID:21150192
Abstract

BACKGROUND/AIMS: Subclinical or frank hypothyroidism is causally implicated in endothelial dysfunction. Since the plasma concentration of the active form of thyroid hormone, triiodothyronine (T₃), is reduced in chronic kidney disease (CKD), where endothelial function is frequently altered, low T₃ may be a factor implicated in this disturbance in CKD patients.

METHODS

We investigated the relationship between flow-mediated vasodilatation (FMD) and thyroid hormones in a series of 217 nondiabetic patients with stage 3-4 CKD.

RESULTS

The plasma concentration of free T₃ (fT₃) was closely associated with FMD (r = 0.38; p < 0.001). fT₃ was also inversely associated with hemoglobin (r = -0.41; p < 0.001), systolic pressure (r = -0.28; p < 0.001) and the plasma concentration of the endogenous inhibitor of NO synthase, asymmetric dimethylarginine (ADMA; r = -0.18; p = 0.007). However, adjustment for ADMA markedly attenuated the fT₃-FMD link, a phenomenon suggesting that raised plasma ADMA, possibly driven by low fT₃, at least in part mediates the adverse effects of low T₃ on endothelial function in CKD.

CONCLUSIONS

Low T₃ in patients with moderate-to-severe CKD is a marker of endothelial dysfunction. This study sets a solid rationale for designing specific intervention studies aimed at clarifying the nature (causal or not causal) of the endothelial function-T₃ link in CKD.

摘要

背景/目的:亚临床或显性甲状腺功能减退症与血管内皮功能障碍有因果关系。由于活性甲状腺激素三碘甲状腺原氨酸(T₃)的血浆浓度在慢性肾脏病(CKD)中降低,而内皮功能在 CKD 中经常改变,因此低 T₃可能是导致 CKD 患者发生这种功能障碍的一个因素。

方法

我们在一系列 217 例非糖尿病 3-4 期 CKD 患者中研究了血流介导的血管舒张(FMD)与甲状腺激素之间的关系。

结果

游离 T₃(fT₃)的血浆浓度与 FMD 密切相关(r = 0.38;p < 0.001)。fT₃ 也与血红蛋白(r = -0.41;p < 0.001)、收缩压(r = -0.28;p < 0.001)和内源性一氧化氮合酶抑制剂不对称二甲基精氨酸(ADMA)的血浆浓度呈负相关(r = -0.18;p = 0.007)。然而,调整 ADMA 后,fT₃-FMD 之间的联系明显减弱,这表明升高的血浆 ADMA,可能是由低 fT₃引起的,至少部分介导了低 T₃对 CKD 内皮功能的不良影响。

结论

中重度 CKD 患者的低 T₃是血管内皮功能障碍的一个标志物。本研究为设计旨在阐明 CKD 中内皮功能与 T₃之间关系的本质(因果关系或非因果关系)的特定干预研究提供了坚实的依据。

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