Perlstein Todd S, Gumieniak Olga, Williams Gordon H, Sparrow David, Vokonas Pantel S, Gaziano Michael, Weiss Scott T, Litonjua Augusto A
Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
Hypertension. 2006 Dec;48(6):1031-6. doi: 10.1161/01.HYP.0000248752.08807.4c. Epub 2006 Oct 23.
Experimental evidence supports a causative role for uric acid in the pathogenesis of hypertension. Prospective studies have variably adjusted for relevant confounders and have been of relatively limited duration. We prospectively examined the relationship between uric acid level and the development of hypertension in the Normative Aging Study, a longitudinal cohort of healthy adult men. Of the 2280 initial men in the Normative Aging Study, 2062 had available information for inclusion in the analysis. Cox proportional hazards model was used to examine the relationship between baseline serum uric acid level and the development of hypertension adjusting for age, body mass index, abdominal circumference, smoking, alcohol, plasma triglycerides, total cholesterol, and plasma glucose. A total of 892 men developed hypertension over a mean of 21.5 years of follow-up. Serum uric acid level independently predicted the development of hypertension in age-adjusted (relative risk [RR]: 1.10; 95% CI: 1.06 to 1.15: P<0.001) and multivariable (RR: 1.05; 95% CI: 1.01 to 1.10; P=0.02) models. Among 1277 men at risk for the development of hypertension at the time of their first serum creatinine measurement, 508 (39.8%) developed hypertension over a mean of 10.3+/-5.5 years of follow-up. Additionally adjusting for calculated glomerular filtration rate in this subset, serum uric acid remained associated with the development of hypertension (RR: 1.06; 95% CI: 1.01 to 1.12; P=0.03). The baseline serum uric acid level is a durable marker of risk for the development of hypertension. The association is independent of elements of the metabolic syndrome, alcohol intake, and renal function.
实验证据支持尿酸在高血压发病机制中起致病作用。前瞻性研究对相关混杂因素进行了不同程度的校正，且研究持续时间相对有限。我们在规范性衰老研究中前瞻性地研究了尿酸水平与高血压发生之间的关系，该研究是一个健康成年男性的纵向队列。在规范性衰老研究最初的2280名男性中，有2062人有可用于分析的信息。采用Cox比例风险模型来研究基线血清尿酸水平与高血压发生之间的关系，并对年龄、体重指数、腹围、吸烟、饮酒、血浆甘油三酯、总胆固醇和血糖进行校正。在平均21.5年的随访中，共有892名男性患高血压。在年龄校正模型（相对风险[RR]：1.10；95%可信区间：1.06至1.15；P<0.001）和多变量模型（RR：1.05；95%可信区间：1.01至1.10；P=0.02）中，血清尿酸水平独立预测高血压的发生。在首次测量血清肌酐时存在高血压发生风险的1277名男性中，508人（39.8%）在平均10.3±5.5年的随访中患高血压。在该亚组中进一步校正计算的肾小球滤过率后，血清尿酸仍与高血压的发生相关（RR：1.06；95%可信区间：1.01至1.12；P=0.03）。基线血清尿酸水平是高血压发生风险的一个持久标志物。这种关联独立于代谢综合征因素、酒精摄入和肾功能。
