肾性高血压治疗专家共识介绍.ppt

* * * * * * * * * * * * * * * * * * * * * * * K/DOQI （即美国国家肾脏病基金会(NKF)肾病患者生存质量指导）在其颁发的慢性肾病高血压和降压药物指南中指出，慢性肾病高血压的降压治疗有3个目的： 1）严格控制血压。 2）保护肾脏,延缓肾病进展。JNC7和2007年发表的欧洲高血压指南对控制血压的具体目标进行了阐述，目标血压应≤130/80mmHg，如果蛋白尿≥1g/天，那么目标血压应该更低。 3）降低心血管疾病危险。 * * * 通过大范围研究设计，患者人群及治疗方案，总结６个大型临床试验中高血压伴主要高危因素（主要为糖尿病）患者平均使用 降压药物的种类。结果一致显示，要想达到目标血压，需要联合使用２种或３种以 上药物。 * * 让我们看一下两种药物联合的机制。 外周血管收缩，外周血流阻力增大，便导致了高血压。使用硝苯地平可以抑制外周血管平滑肌收缩，导致外周血管舒张，从而引起血压下降。但血压下降后便会通过刺激压力感受器激活RAAS和SNS，引起醛固酮和Angll水平增加，引起外周血管收缩。联合使用ACEI可以降低Angll的浓度，降低外周血管阻力。所以，联合用药能更有效的降压控压。 * * 让我们一起了解一下CCB在肾脏内科高血压治疗中的应用。 * * * ACE inhibitors interfere with the pathophysiology of coronary ischaemia and renal insufficiency through blockade of the renin-angiotensin system (Willenheimer et al 1999). In adult tissues, virtually all known deleterious effects of angiotensin II (AII) ? the end product of the renin-angiotensin system ? are attributable to the AT1 receptor (Dahl?f 1995). The adverse cerebral and cardiovascular effects of AII, which have potentially lethal sequelae, are pervasive. Preclinical data implicate A II in cerebro-vascular ischaemia through the development of atherosclerosis (Daugherty et al 2000). By potentiating the activity of other neurohormonal systems, AII exerts harmful cardiovascular effects by means of the AT1 receptor (Willenheimer et al 1999) ? including vasoconstriction (Willenheimer et al 1999), vascular hypertrophy (Fyhrquist et al 1995), left ventricular hypertrophy (Fyhrquist et al 1995), myocardial and vascular wall fibrosis (Willenheimer et al 1999), myocardial remodeling (Fyhrquist et al 1995), and cardiac myocyte apoptosis under some conditions (Booz Baker 1998) ? and thereby contributes to the development of hypertension, heart failure, and myocardial infarction (Dahl?f 1995; Fyhrquist et al 1995). AII also plays a central role in the development of renal insufficiency in response to heart failure. As cardiac function deteriorates, decreased renal blood flow leads to a reduced glomerular fi