Inflammation and Apparent Treatment-Resistant Hypertension in Patients With Chronic Kidney Disease The Results From the CRIC Study

Inflammation and Apparent Treatment-Resistant Hypertension in Patients With Chronic Kidney Disease The Results From the CRIC Study
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DOI:
10.1161/hypertensionaha.118.12358
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发表时间:
2019-04-01
期刊:
影响因子:
8.3
通讯作者:
Townsend, Raymond R.
Townsend, Raymond R.
中科院分区:
医学1区
文献类型:
--
作者:
Chen, Jing;Bundy, Joshua D.;Townsend, Raymond R.

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显性治疗抵抗性高血压(ATRH)在慢性肾病患者中非常普遍,并与心血管疾病风险相关。我们分析了慢性肾脏疾病患者炎症生物标志物与ATRH及其并发症的关系。ATRH定义为服用降压药>= 3或降压药降压4时血压>= 140/90 mm Hg。分析纳入了1359例慢性肾功能不全队列(Chronic Renal dysfunction Cohort, CRIC)的ATRH患者和2008例无ATRH的高血压患者。使用逻辑回归来检查炎症生物标志物和ATRH的横断面关联,调整人口统计学、生活方式、临床危险因素和治疗方法。使用Cox比例风险模型来评估炎症生物标志物对ATRH与复合心血管疾病和死亡率的关联的影响。炎症生物标志物水平最高分位数与最低分位数的ATRH比值比(95% CI) IL(白细胞介素)-6为1.29 (95% CI, 1.05-1.59), tnf - α(肿瘤坏死因子- α)为1.49 (95% CI, 1.20-1.85), tgf - β(转化生长因子- β)为0.77 (95% CI, 0.63-0.95)。高敏CRP (c反应蛋白)、纤维蛋白原、IL-1 β和IL-1受体拮抗剂与ATRH无显著相关性。在Cox模型中加入炎症生物标志物并没有减弱ATRH与心血管疾病和死亡率的显著相关性。我们的研究结果表明,较高水平的IL-6和tnf - α和较低水平的tgf - β与ATRH的几率独立相关。针对特定炎症途径可能改善慢性肾脏疾病患者的血压控制。
Apparent treatment-resistant hypertension (ATRH) is highly prevalent and associated with cardiovascular disease risk in patients with chronic kidney disease. We analyzed the association of inflammatory biomarkers with ATRH and its complications in patients with chronic kidney disease. ATRH was defined as blood pressure >= 140/90 mm Hg while taking >= 3 antihypertensive medications or blood pressure = 4 medications. Analyses included 1359 CRIC study (Chronic Renal Insufficiency Cohort) participants with ATRH and 2008 hypertensive participants without. Logistic regression was used to examine cross-sectional associations of inflammatory biomarkers and ATRH adjusting for demographic, lifestyle, and clinical risk factors and treatments. Cox proportional hazards models were used to assess the impact of inflammatory biomarkers on associations of ATRH with composite cardiovascular disease and mortality beyond conventional risk factors. Multivariable-adjusted odds ratio (95% CI) of ATRH for the highest tertile versus the lowest tertile of inflammatory biomarker levels was 1.29 (95% CI, 1.05-1.59) for IL (interleukin)-6, 1.49 (95% CI, 1.20-1.85) for TNF-alpha (tumor necrosis factor-alpha), and 0.77 (95% CI, 0.63-0.95) for TGF-beta (transforming growth factor-beta). High-sensitivity CRP (C-reactive protein), fibrinogen, IL-1 beta, and IL-1 receptor antagonist were not significantly associated with ATRH. Adding inflammatory biomarkers to Cox models did not attenuate the significant association of ATRH with cardiovascular disease and mortality. Our findings show higher levels of IL-6 and TNF-alpha and lower levels of TGF-beta were independently associated with odds of ATRH. Targeting specific inflammatory pathways may improve blood pressure control in patients with chronic kidney disease.