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肾素-血管紧张素-醛固酮系统阻断在高血压和糖尿病中发挥肾脏保护作用的证据。

Evidence for renoprotection by blockade of the renin-angiotensin-aldosterone system in hypertension and diabetes.

作者信息

Karalliedde J, Viberti G

机构信息

Unit for Metabolic Medicine, Department of Diabetes, Endocrinology and Internal Medicine, Cardiovascular Division, King's College London School of Medicine, King's College London, London, UK.

出版信息

J Hum Hypertens. 2006 Apr;20(4):239-53. doi: 10.1038/sj.jhh.1001982.

DOI:10.1038/sj.jhh.1001982
PMID:16452996
Abstract

The incidence of end-stage renal disease (ESRD) is rising worldwide, accompanied by corresponding increases in the risk of morbidity and mortality. Underlying this trend are increasing rates of hypertension and diabetes mellitus, the two most common causes of ESRD. In addition to the adverse haemodynamic effects of hypertension on the kidney, elevated blood pressure (BP) can activate components of the renin-angiotensin-aldosterone system (RAAS), which, in turn, activate mediators of inflammation, oxidative stress, cell growth, and matrix accumulation. Lowering BP reduces the risk of cardiovascular events and renal damage. Accumulating evidence from clinical and laboratory studies suggests that interrupting the RAAS with therapies such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and aldosterone receptor blockers can interfere with the mechanisms that promote diabetic and non-diabetic renal damage. Moreover, clinical trials of RAAS blockade have demonstrated reductions in microalbuminuria, a predictor of increased cardiorenal risk and overt nephropathy in patients with and without diabetes and/or hypertension. In this way, agents that block the RAAS should be considered the drugs of first choice as they provide enhanced renoprotection compared with other classes of antihypertensive agents such as calcium channel blockers and beta-blockers.

摘要

终末期肾病(ESRD)的发病率在全球范围内呈上升趋势,同时发病和死亡风险也相应增加。导致这一趋势的根本原因是高血压和糖尿病发病率的上升,这两种疾病是ESRD最常见的病因。除了高血压对肾脏产生不良血流动力学影响外,血压升高(BP)还可激活肾素-血管紧张素-醛固酮系统(RAAS)的组成部分,进而激活炎症、氧化应激、细胞生长和基质积聚的介质。降低血压可降低心血管事件和肾损伤的风险。临床和实验室研究积累的证据表明,使用血管紧张素转换酶抑制剂、血管紧张素II受体阻滞剂和醛固酮受体阻滞剂等疗法阻断RAAS,可干扰促进糖尿病和非糖尿病肾损伤的机制。此外,RAAS阻断的临床试验表明,微量白蛋白尿有所减少,微量白蛋白尿是糖尿病和非糖尿病患者及高血压患者发生心肾风险增加和显性肾病的预测指标。因此,与其他类别的抗高血压药物(如钙通道阻滞剂和β受体阻滞剂)相比,阻断RAAS的药物应被视为首选药物,因为它们能提供更强的肾脏保护作用。

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