原发性高血压患者降压治疗中微量白蛋白尿发生的相关因素

J. Redón, E. Rovira, A. Miralles, R. Julve, J. Pascual
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引用次数: 57

摘要

该研究的目的是评估在未接受过治疗的原发性高血压年轻成人随访期间微量白蛋白尿发生的相关因素。正常蛋白尿原发性高血压患者,年龄<50岁,既往未接受过降压药治疗,且无糖尿病。初步评估后,患者仅使用非药物措施(n=62), &bgr;阻滞剂(n=38), ACE抑制剂(n=64),钙通道阻滞剂(n=8)和几种药物(n=15)进行治疗。在研究开始时测量办公室血压、生化特征和24小时尿白蛋白排泄量,并在平均2.7±1.2年的随访期间每年测量一次。在纳入的187例患者中,22例(11.7%)发生微量白蛋白尿(进展者,4.4/100例/年)。在年龄、性别、体重指数、病程、血压值、生化特征、糖尿病或高血压家族史、吸烟习惯或EKG左心室肥厚的存在方面,进展者和保持正常蛋白尿(非进展者)之间没有差异。进展率最低的组为ACE抑制剂治疗组(n=5;2.9/100例/y),其次为饮食组(n=5;3.3/100例/y)和&bgr;受体阻滞剂组(n=5;4.1/100的患者/ y)。当我们排除接受钙通道阻滞剂治疗的患者或在不同治疗类别之间随时间变化的患者时,在组间观察到微量白蛋白尿发生率无显著差异。与非进展者相比,进展者的空腹血糖斜率(4.78±11.4比0.50±6.8 mg/y, P <0.02)和尿酸斜率(0.58±0.93比0.05±1.10 mg/y, P <0.03)更高。血糖和收缩压随时间的斜率都与尿白蛋白排泄对数的斜率独立相关,当对年龄、性别和治疗组进行调整时。微量白蛋白尿进展的Cox比例风险模型显示,基线尿白蛋白排泄(风险比[RR]=1.06;置信区间[CI] 95%, 1.01 ~ 1.11),收缩压斜率(RR=1.11;CI 95%, 1.03 ~ 1.20),葡萄糖的斜率(RR=1.08;可信区间95%,1.03 - 1.14)与微量白蛋白尿的发生独立相关。综上所述,在一组未接受过治疗的年轻原发性高血压患者中,在降压治疗期间影响微量白蛋白尿发生的主要因素是基线时的微量白蛋白尿值以及收缩压和空腹血糖的斜率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Factors Related to the Occurrence of Microalbuminuria During Antihypertensive Treatment in Essential Hypertension
The objective of the study was to assess the factors related to the occurrence of microalbuminuria during the follow-up of a young adult group with essential hypertension that had not been previously treated. Normo-albuminuric essential hypertensives, <50 years old, who had not been previously treated with antihypertensive drugs and who did not have diabetes mellitus were included. After the initial evaluation, patients were treated using only nonpharmacological measures (n=62), &bgr;-blockers (n=38), ACE inhibitors (n=64), calcium channel blockers (n=8), and several classes (n=15). Measurements were taken for office blood pressure, biochemical profile, and 24-hour urinary albumin excretion at the beginning of the study and were measured yearly during an average of 2.7±1.2 years of follow-up. Among the 187 patients included, 22 (11,7%) developed microalbuminuria (progressors, 4.4/100 patients/y). No differences were present between progressors and those who remained normo-albuminuric (nonprogressors) in terms of age, gender, body mass index, disease duration, blood pressure values, biochemical profile, familial history of diabetes or hypertension, smoking habits, or the presence of EKG left ventricular hypertrophy. The group with the lowest progression rate was the patients treated with ACE inhibitors (n=5; 2.9/100 patients/y), followed by the diet group (n=5; 3.3/100 patients/y) and the &bgr;-blockers group (n=5; 4.1/100 patients/y). When we excluded patients treated with calcium channel blockers or those who changed over time between different classes of treatment, no significant differences in the incidence of microalbuminuria were observed among the groups. Progressors showed higher slopes of fasting glucose (4.78±11.4 versus 0.50±6.8 mg/y, P <0.02) and uric acid (0.58±0.93 versus 0.05±1.10 mg/y, P <0.03) compared with the slopes of nonprogressors. Both the slopes for glucose and systolic blood pressure over time were associated independently with the slope of the logarithm of urinary albumin excretion when adjusted for age, gender, and treatment groups. Cox proportional hazard model for progression of microalbuminuria showed that baseline urinary albumin excretion (risk ratio [RR]=1.06; confidence interval [CI] 95%, 1.01 to 1.11), slope for systolic blood pressure (RR=1.11; CI 95%, 1.03 to 1.20), and slope for glucose (RR=1.08; CI 95%, 1.03 to 1.14) were independently associated to the development of microalbuminuria. In conclusion, in a group of young adults with essential hypertension that had not been previously treated, the main factors influencing the occurrence of microalbuminuria during antihypertensive treatment were the values of microalbuminuria at baseline and the slopes for systolic blood pressure and fasting glucose.
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