Relationship between endothelial dysfunction and kidney disease.
Relationship between endothelial dysfunction and kidney disease.
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内皮功能障碍与肾脏疾病的关系。
DOI：
10.1111/jch.12236
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发表时间：
2014
影响因子：
2.8
通讯作者：
et al.
中科院分区：
文献类型：
--
作者：
Kabutoya T;et al.
我们感谢巴尔塔博士和同事们对我们工作的兴趣，并希望对他们最近的文章做出回应。2我们同意调查隐匿性高血压（MHT）患者病理状态的重要性，包括炎症标志物。我们重新分析了内皮功能障碍（即，血流介导的血管舒张[FMD]幅度[DFMD]和积分FMD反应[FMD-AUC 120]）与其他病理状态之间的相关性。我们还在研究中测量了尿白蛋白-肌酐比值（UACR）3，4（表）。持续性高血压患者的尿肌酐清除率（办公室血压[BP]≥ 140/90 mm Hg和家庭血压≥ 135/85 mm Hg）显著高于两种白大衣高血压患者血压正常者（办公室血压<140/90 mmHg，家庭血压<135/85 mmHg）。MHT组UACR与正常血压组相比差异无统计学意义，但其潜在原因可能是II型错误。这一发现与我们以前的研究结果相似。5 FMD-AUC 120与log UACR显着负相关（r= ± 0. 18，P=. 008），但DFMD与log UACR无关（r= 0.008）。06，P=. 35）。FMDAUC 120反映肾脏疾病，但DFMD没有。FMD-AUC 120最低三分位数患者（FMD-AUC 120 < 5.0 mmxs，n= 86）的UACR显著高于FMD-AUC 120最高三分位数患者（FMD-AUC 120 ≥ 11.0 mmxs，n= 86）[P<0.05]。001];图，图A），但DFMD的最低和最高三分位数患者的UACR相似（P= 1.0;图，图B）。我们没有评估久坐习惯或肝功能。我们测量了高敏C反应蛋白（hsCRP）水平，但log-hsCRP与DFMD或FMD-AUC 120无关。正如Balba博士所评论的，1内皮功能障碍，测量为FMD（不是DFMD，而是FMDAUC 120），可能与肾脏疾病有关。然而，在我们的患者人群中，FMD和炎症之间没有关联。我们先前证明FMD-AUC 120与Frachial风险评分相关，3和进一步的研究
We thank Dr Balta and colleagues1 for their interest in our work, and would like to respond to their recent article. 2 We agree concerning the importance of investigating the pathological status in patients with masked hypertension (MHT), including inflammation markers. We reanalyzed the association between endothelial dysfunction (ie, the flow-mediated vasodilation [FMD] magnitude [DFMD] and the integrated FMD response [FMD-AUC120]) and other pathological status. We also measured the urinary albumin-creatinine ratio (UACR) in our studies3, 4 (Table). The UACR in the patients with sustained hypertensive (office blood pressure [BP]≥ 140/90 mm Hg and home BP≥ 135/85 mm Hg) was significantly higher than that among both the patients with white-coat hypertension (office BP≥ 140/90 mm Hg and home BP< 135/85 mm Hg) and the patients with normotension (office BP< 140/90 mm Hg and home BP< 135/85 mm Hg). The differences in UACR in the MHT group and those in the normotensive patients were not statistically significant, but the underlying reason might be a type II error. This finding was similar to that obtained in our previous study. 5 FMD-AUC120 was significantly inversely associated with log UACR (r= À0. 18, P=. 008), but DFMD was not associated with log UACR (r= À0. 06, P=. 35). FMDAUC120 reflected kidney disease, but DFMD did not. The UACR was significantly higher in the patients in the lowest tertile for FMD-AUC120 (FMD-AUC120< 5.0 mmxs, n= 86) than in the patients in the highest tertile for FMD-AUC120 (FMD-AUC120≥ 11.0 mmxs, n= 86 [P<. 001]; Figure, panel A), but the UACR was similar in the patients in the lowest and highest tertiles for DFMD (P= 1.0; Figure, panel B). We did not evaluate sedentary habits or liver function. We measured the high-sensitivity CRP (hsCRP) level, but log-hsCRP was not associated with DFMD or with FMD-AUC120.As Dr Balba commented, 1 endothelial dysfunction, which was measured as FMD (not DFMD, but FMDAUC120), might be associated with kidney disease. However, in our patient population, there was no association between FMD and inflammation. We previously demonstrated that FMD-AUC120 was associated with the Framingham risk score, 3 and further studies