Primary aldosteronism is recognized as a severe form of renin-independent aldosteronism that results in excessive mineralocorticoid receptor (MR) activation.

To investigate whether a spectrum of subclinical renin-independent aldosteronism that increases risk for hypertension exists among normotensive persons.

Cohort study.

National community-based study.

850 untreated normotensive participants in MESA (Multi-Ethnic Study of Atherosclerosis) with measurements of serum aldosterone and plasma renin activity (PRA).

Longitudinal analyses investigated whether aldosterone concentrations, in the context of physiologic PRA phenotypes (suppressed, ≤0.50 µg/L per hour; indeterminate, 0.51 to 0.99 µg/L per hour; unsuppressed, ≥1.0 µg/L per hour), were associated with incident hypertension (defined as systolic blood pressure ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of antihypertensive medications). Cross-sectional analyses investigated associations between aldosterone and MR activity, assessed via serum potassium and urinary fractional excretion of potassium.

A suppressed renin phenotype was associated with a higher rate of incident hypertension than other PRA phenotypes (incidence rates per 1000 person-years of follow-up: suppressed renin phenotype, 85.4 events [95% CI, 73.4 to 99.3 events]; indeterminate renin phenotype, 53.3 events [CI, 42.8 to 66.4 events]; unsuppressed renin phenotype, 54.5 events [CI, 41.8 to 71.0 events]). With renin suppression, higher aldosterone concentrations were independently associated with an increased risk for incident hypertension, whereas no association between aldosterone and hypertension was seen when renin was not suppressed. Higher aldosterone concentrations were associated with lower serum potassium and higher urinary excretion of potassium, but only when renin was suppressed.

Sodium and potassium were measured several years before renin and aldosterone.

Suppression of renin and higher aldosterone concentrations in the context of this renin suppression are associated with an increased risk for hypertension and possibly also with increased MR activity. These findings suggest a clinically relevant spectrum of subclinical primary aldosteronism (renin-independent aldosteronism) in normotension.

National Institutes of Health.

原发性醛固酮增多症被认为是一种严重的不依赖肾素的醛固酮增多症，会导致盐皮质激素受体 (MR) 过度激活。

调查是否存在一系列亚临床肾素非依赖性醛固酮增多症会增加血压正常人群的高血压风险。

队列研究。

国家社区研究。

在 MESA（动脉粥样硬化的多种族研究）中，850 名未经治疗的血压正常参与者测量了血清醛固酮和血浆肾素活性 (PRA)。

纵向分析调查了在生理 PRA 表型（抑制，≤0.50 µg/L/小时；不确定，0.51 至 0.99 µg/L/小时；未抑制，≥1.0 µg/L/小时）的情况下，醛固酮浓度是否与突发高血压（定义为收缩压≥140 mm Hg，舒张压≥90 mm Hg，或开始服用抗高血压药物）。横断面分析调查了醛固酮和 MR 活性之间的关联，通过血清钾和尿钾排泄分数进行评估。

与其他 PRA 表型相比，抑制的肾素表型与更高的高血压发病率相关（每 1000 人年随访的发病率：抑制的肾素表型，85.4 次事件 [95% CI，73.4 至 99.3 次事件]；不确定的肾素表型, 53.3 事件 [CI, 42.8 至 66.4 事件]；未抑制的肾素表型，54.5 事件 [CI, 41.8 至 71.0 事件]）。对于肾素抑制，较高的醛固酮浓度与发生高血压的风险增加独立相关，而当肾素未受到抑制时，醛固酮与高血压之间没有关联。较高的醛固酮浓度与较低的血清钾和较高的尿钾排泄相关，但仅在肾素被抑制时。

在肾素和醛固酮之前几年测量钠和钾。

在这种肾素抑制的情况下，肾素的抑制和较高的醛固酮浓度与高血压风险的增加以及可能与 MR 活性的增加有关。这些发现表明在血压正常时存在临床相关的亚临床原发性醛固酮增多症（肾素非依赖性醛固酮增多症）谱。

美国国立卫生研究院。