UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8523, USA.
Clin J Am Soc Nephrol. 2011 Aug;6(8):2016-24. doi: 10.2215/CJN.11351210. Epub 2011 Jul 14.
Intradialytic hypertension is associated with adverse outcomes, yet the mechanism is uncertain. Patients with intradialytic hypertension exhibit imbalances in endothelial-derived vasoregulators nitric oxide and endothelin-1, indirectly suggesting endothelial cell dysfunction. We hypothesized that intradialytic hypertension is associated in vivo with endothelial cell dysfunction, a novel predictor of adverse cardiovascular outcomes.
DESIGN, SETTINGS, PARTICIPANTS, & MEASUREMENTS: We performed a case-control cohort study including 25 hemodialysis (HD) subjects without (controls) and 25 with intradialytic hypertension (an increase in systolic BP pre- to postdialysis ≥10 mmHg ≥4/6 consecutive HD sessions). The primary outcome was peripheral blood endothelial progenitor cells (EPCs) assessed by aldehyde dehydrogenase activity (ALDH(br)) and cell surface marker expression (CD34(+)CD133(+)). We also assessed endothelial function by ultrasonographic measurement of brachial artery flow-mediated vasodilation (FMD) normalized for shear stress. Parametric and nonparametric t tests were used to compare EPCs, FMD, and BP.
Baseline characteristics and comorbidities were similar between groups. Compared with controls, 2-week average predialysis systolic BP was lower among subjects with intradialytic hypertension (144.0 versus 155.5 mmHg), but postdialysis systolic BP was significantly higher (159.0 versus 128.1 mmHg). Endothelial cell function was impaired among subjects with intradialytic hypertension as measured by decreased median ALDH(br) cells and decreased CD34(+)CD133(+) cells (ALDH(br), 0.034% versus 0.053%; CD34(+)CD133(+), 0.033% versus 0.059%). FMD was lower among subjects with intradialytic hypertension (1.03% versus 1.67%).
Intradialytic hypertension is associated with endothelial cell dysfunction. We propose that endothelial cell dysfunction may partially explain the higher event rates observed in these patients.
透析中高血压与不良预后相关，但具体机制尚不清楚。透析中高血压患者表现出内皮衍生血管调节因子一氧化氮和内皮素-1的失衡，这间接表明内皮细胞功能障碍。我们假设透析中高血压与内皮细胞功能障碍相关，而内皮细胞功能障碍是心血管不良结局的一个新的预测因子。
设计、地点、参与者和测量方法：我们进行了一项病例对照队列研究，纳入了 25 名无透析中高血压（对照组）和 25 名有透析中高血压（透析前至透析后收缩压升高≥10mmHg，≥4/6 次连续 HD 治疗）的血液透析（HD）患者。主要结局是通过醛脱氢酶活性（ALDH(br)）和细胞表面标志物表达（CD34(+)CD133(+)）评估外周血内皮祖细胞（EPCs）。我们还通过超声测量肱动脉血流介导的血管扩张（FMD）来评估内皮功能，并用剪切力进行标准化。使用参数和非参数 t 检验比较 EPCs、FMD 和血压。
两组的基线特征和合并症相似。与对照组相比，透析中高血压患者的 2 周平均预透析收缩压较低（144.0 与 155.5mmHg），但透析后收缩压明显较高（159.0 与 128.1mmHg）。通过降低中位数 ALDH(br)细胞和降低 CD34(+)CD133(+)细胞（ALDH(br)，0.034%与 0.053%；CD34(+)CD133(+)，0.033%与 0.059%），透析中高血压患者的内皮细胞功能受损。透析中高血压患者的 FMD 较低（1.03%与 1.67%）。
透析中高血压与内皮细胞功能障碍相关。我们提出，内皮细胞功能障碍可能部分解释了这些患者更高的事件发生率。
