Mater Research Institute, The University of Queensland, Brisbane, Queensland, Australia.
Menzies Research Institute, Griffith University, Gold Coast, Queensland, Australia.
Am J Hypertens. 2017 Nov 6;30(12):1196-1202. doi: 10.1093/ajh/hpx123.
Subjects with hypertension are frequently obese or insulin resistant, both conditions in which hyperuricemia is common. Obese and insulin-resistant subjects are also known to have blood pressure that is more sensitive to changes in dietary sodium intake. Whether hyperuricemia is a resulting consequence, moderating or contributing factor to the development of hypertension has not been fully evaluated and very few studies have reported interactions between sodium intake and serum uric acid.
We performed further analysis of our randomized controlled clinical trials (Australian New Zealand Clinical Trials Registry #12609000161224 and #12609000292279) designed to assess the effects of modifying sodium intake on concentrations of serum markers, including uric acid. Uric acid and other variables (including blood pressure, renin, and aldosterone) were measured at baseline and 4 weeks following the commencement of low (60 mmol/day), moderate (150 mmol/day), and high (200-250 mmol/day) dietary sodium intake.
The median aldosterone-to-renin ratio was 1.90 [pg/ml]/[pg/ml] (range 0.10-11.04). Serum uric acid fell significantly in both the moderate and high interventions compared to the low sodium intervention. This pattern of response occurred when all subjects were analyzed, and when normotensive or hypertensive subjects were analyzed alone.
Although previously reported in hypertensive subjects, these data provide evidence in normotensive subjects of an interaction between dietary sodium intake and serum uric acid. As this interaction is present in the absence of hypertension, it is possible it could play a role in hypertension development, and will need to be considered in future trials of dietary sodium intake.
The trials were registered with the Australian and New Zealand Clinical Trials Registry as ACTRN12609000161224 and ACTRN1260.
高血压患者通常肥胖或存在胰岛素抵抗，这两种情况都很常见高尿酸血症。肥胖和胰岛素抵抗的患者的血压对饮食钠摄入的变化也更为敏感。高尿酸血症是高血压发展的结果、调节因素还是促成因素，尚未得到充分评估，很少有研究报告钠摄入与血清尿酸之间的相互作用。
我们对我们的随机对照临床试验进行了进一步分析（澳大利亚新西兰临床试验注册处 #12609000161224 和 #12609000292279），旨在评估改变钠摄入量对血清标志物（包括尿酸）浓度的影响。在开始低（60mmol/天）、中（150mmol/天）和高（200-250mmol/天）饮食钠摄入后 4 周，测量尿酸和其他变量（包括血压、肾素和醛固酮）。
中位数醛固酮-肾素比值为 1.90[pg/ml]/[pg/ml]（范围 0.10-11.04）。与低钠干预相比，中钠和高钠干预均使血清尿酸显著降低。当分析所有受试者时以及当分析正常血压或高血压受试者时，均观察到这种反应模式。
尽管先前在高血压患者中报道过，但这些数据为正常血压受试者中饮食钠摄入与血清尿酸之间的相互作用提供了证据。由于这种相互作用在没有高血压的情况下存在，因此它可能在高血压发展中发挥作用，需要在未来的饮食钠摄入试验中加以考虑。
这些试验在澳大利亚和新西兰临床试验注册处注册为 ACTRN12609000161224 和 ACTRN1260。
