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肾脏病与透析肾移植杂志 ›› 2012, Vol. 21 ›› Issue (3): 217-222.

• 论文 • 上一篇    下一篇

血管紧张素转换酶抑制剂和血管紧张素Ⅱ受体阻断剂单药治疗及联合应用对慢性肾脏病患者肾素-血管紧张素系统表达的影响

  

  • 出版日期:2012-06-28 发布日期:2012-06-25

Effect of angiotensin converting enzyme inhibitor and angiotensin Ⅱ receptor blocker on renin-angiotensin system in patients with chronic kidney disease

  • Online:2012-06-28 Published:2012-06-25

摘要:

摘 要  目的:探讨血管紧张素转换酶抑制剂(ACEI)和血管紧张素Ⅱ受体阻断剂(ARB)单药治疗及联合应用对慢性肾脏病(CKD)患者循环和肾脏局部肾素-血管紧张素系统(RAS)表达的影响及差异。方法:采用前瞻性随机对照设计,将24例CKD患者随机分为贝那普利组、缬沙坦组和联合治疗组,分别予贝那普利20mg/d、缬沙坦160mg/d、贝那普利10mg/d和缬沙坦80mg/d治疗8周。记录随访过程中的血压、SCr、蛋白尿等临床指标,并采用放射免疫法和酶联免疫吸附法测定血和尿RAS组分,比较治疗前后的临床指标和血、尿RAS组分活性以及三组间的差异。结果:治疗8周后贝那普利组的蛋白尿[(0.61±0.25) g/24h vs (0.35±0.20)g/24h, P<0.05)、尿血管紧张素原 [(60.76±28.05)ng/(mg Cr) vs (23.09±14.74)ng/(mg Cr), P<0.05]低于基线;缬沙坦组的平均动脉压低于基线[(99.17±10.56) mmHg vs (84.63±9.33)mmHg, P<0.05],血浆肾素活性(PRA)高于基线[(1.33±0.76) ng/(ml.h) vs (6.02±2.59)ng/(ml.h), P<0.01]。贝那普利组、缬沙坦和联合治疗组的主要终点事件发生率(蛋白尿下降大于30%)分别为87.5%、12.5%和62.5%,贝那普利组显著高于缬沙坦组(P<0.05)。治疗8周后贝那普利组PRA [(3.20±1.25) ng/(ml.h) vs (6.02±2.59)ng/(ml.h), P<0.05)和血管紧张素Ⅱ浓度[(53.32±11.13) pg/ml vs (105.61±59.49)pg/ml, P<0.05)低于缬沙坦组。结论:贝那普利短期治疗可有效降低慢性肾脏病患者肾脏局部血管紧张素Ⅱ活性和蛋白尿,而缬沙坦可较贝那普利更显著升高血浆肾素活性和血管紧张素Ⅱ浓度。

关键词: 血管紧张素转换酶抑制剂, 血管紧张素Ⅱ受体阻断剂, 蛋白尿, 血管紧张素原, 血浆肾素活性, 血管紧张素Ⅱ

Abstract:

ABSTRACT  Objective:To investigate the effect of angiotensin converting enzyme inhibitor(ACEI), angiotensin Ⅱ receptor blocker(ARB) and combined treatment on general and intrarenal renin-angiotensin system(RAS) in pants with chronic kidney disease(CKD). Methodology:Twenty-four CKD patients were randomly assigned to benazepril, valsartan or conmbined treatment group. During 8 weeks of benazepril treatment (20mg/d), valsartan treatment (160mg/d) or conmbined treatment (benazepril 10mg/d and valsartan 80mg/d), the blood pressure, serum creatinine, and proteinuria were detected, and the plasma renin activity (PRA), plasma and urinary angiotensinogen(AGT), angiotensin Ⅱ(Ang Ⅱ) and aldosterone were measured by RIA or ELISA. Results:After treatment of 8 weeks, the level of proteinuria [(0.61±0.25)g/24h vs (0.35±0.20)g/24h, P<0.05] and urinary AGT [(60.76±28.05) ng/ (mg Cr) vs (23.09±14.74) ng/ (mg Cr), P<0.05] was lower in benazepril group than that in baseline. In valsartan group, mean artery pressure was lower than baseline [(99.17±10.56)mmHg vs (84.63±9.33)mmHg, P<0.05] and PRA was higher than baseline[ (1.33±0.76) ng/(ml.h) vs (6.02±2.59)ng/(ml.h), P<0.01]. The primary end point was 87.5% in benazepril group, 12.5% in valsartan group and 62.5% in combined treatment group. Compared with valsartan, the primary end point was reduced by benazepril (P<0.05). After 8 weeks treatment, PRA [(3.20±1.25)ng/(ml.h) vs (6.02±2.59)ng/(ml.h), P<0.05] and plasma Ang Ⅱ [(53.32±11.13)pg/ml vs (105.61±59.49)pg/ml, P<0.05] of benazepril group were lower than those of valsartan group. Conclusion: Short-term treatment with benazepril can reduce intrarenal agiotensin Ⅱ activity and urinary protein in patients with CKD. Valsartan may elevate plasma renin activity and angiotensin Ⅱ more significantly than benazepril.

Key words: Angiotensin converting enzyme inhibitor, Angiotensin Ⅱ receptor blocker, Proteinuria, Angiotensinogen, Plasma renin activity, Angiotensin Ⅱ