Continuum of Renin-Independent Aldosteronism in Normotension.
Continuum of Renin-Independent Aldosteronism in Normotension.
复制标题
DOI：
10.1161/hypertensionaha.116.08952
复制
发表时间：
2017-05
期刊：
影响因子：
--
通讯作者：
Vaidya A
中科院分区：
文献类型：
--
作者：
Baudrand R;Guarda FJ;Fardella C;Hundemer G;Brown J;Williams G;Vaidya A
原发性醛固酮增多症（PA）是自主性醛固酮增多症的一种严重形式。较轻微的自主性且不依赖肾素的醛固酮增多症形式可能很常见，甚至在血压正常的人群中也是如此。我们对210名血压正常且血浆肾素活性受抑制（PRA<1.0 ng/mL/小时）的个体的醛固酮分泌情况进行了研究，这些人完成了口服钠抑制试验，接受了血管紧张素II（AngII）输注，并测量了血压（BP）和肾血浆流量（RPF）。我们还研究了尿醛固酮排泄率（AER）、肾素和钾处理之间的连续相关性。根据公认的标准，即尿钠排泄>200 mmol/24小时且AER>12 mcg/24小时，确定了与确诊的PA相符的严重自主性醛固酮分泌。在整个人群中，较高的AER与较高的尿钾排泄、较高的AngII刺激的醛固酮以及较低的PRA之间存在强烈且显著的相关性，这表明存在不依赖肾素的醛固酮增多症和盐皮质激素受体活性的连续谱系。在29名参与者（14%）中检测到符合PA确诊标准的自主性醛固酮分泌。有证据提示确诊为PA的血压正常者正如预期的那样，具有较高的24小时尿AER（20.2±12.2比6.2±2.9 mcg/24小时，P<0.001），但也有较高的AngII刺激的醛固酮（12.4±8.6比6.6±4.3 ng/dL，P<0.001）以及较低的24小时尿钠钾排泄比（2.69±0.65比3.69±1.50 mmol/mmol，P = 0.001）；然而，两组之间在年龄、醛固酮与肾素比值、血压或肾血浆流量方面没有差异。这些发现表明在血压正常人群中存在不依赖肾素的醛固酮增多症和盐皮质激素受体活性的连续谱系，其范围从轻微到明显失调和自主。需要进行纵向研究以确定这种自主性醛固酮分泌谱系是否会导致高血压和心血管疾病。
Primary aldosteronism (PA) is a severe form of autonomous aldosteronism. Milder forms of autonomous and renin-independent aldosteronism may be common, even in normotension. We characterized aldosterone secretion in 210 normotensives who had suppressed plasma renin activity (PRA<1.0 ng/mL/h), completed an oral sodium suppression test, received an infusion of angiotensin II (AngII), and had measurements of blood pressure (BP) and renal plasma flow (RPF). Continuous associations between urinary aldosterone excretion rate (AER), renin, and potassium handling were investigated. Severe autonomous aldosterone secretion that was consistent with confirmed PA was defined based on accepted criteria of an AER >12 mcg/24h with urinary sodium excretion >200 mmol/24h. Across the population, there were strong and significant associations between higher AER and higher urinary potassium excretion, higher AngII-stimulated aldosterone, and lower PRA, suggesting a continuum of renin-independent aldosteronism and mineralocorticoid receptor activity. Autonomous aldosterone secretion that fulfilled confirmatory criteria for PA was detected in 29 participants (14%). Normotensives with evidence suggestive of confirmed PA had higher 24h urinary AER (20.2±12.2 vs. 6.2±2.9 mcg/24h, P<0.001) as expected, but also higher AngII-stimulated aldosterone (12.4±8.6 vs. 6.6±4.3 ng/dL, P<0.001) and lower 24h urinary sodium-to-potassium excretion (2.69±0.65 vs. 3.69±1.50 mmol/mmol, P=0.001); however, there were no differences in age, aldosterone-to-renin ratio, BP, or RPF between the two groups. These findings indicate a continuum of renin-independent aldosteronism and mineralocorticoid receptor activity in normotension that ranges from subtle to overtly dysregulated and autonomous. Longitudinal studies are needed to determine whether this spectrum of autonomous aldosterone secretion contributes to hypertension and cardiovascular disease.