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肾素非依赖性醛固酮增多症的一种严重形式，会导致盐皮质激素受体 (MR) 过度激活。

旨在调查血压正常人群中是否存在一系列亚临床肾素依赖性醛固酮增多症，这些醛固酮增多症会增加高血压的风险。

 队列研究。

国家社区研究。

MESA（动脉粥样硬化多种族研究）中的 850 名未经治疗的正常血压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，每小时 ≤0.50 µg/L；不确定，每小时 0.51 至 0.99 µg/L；未抑制，每小时 ≥1.0 µg/L）背景下醛固酮浓度是否与高血压事件（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）。横断面分析研究了醛固酮和 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，肾素表型抑制与较高的高血压发生率相关（每 1000 人年随访发病率：肾素表型抑制，85.4 起事件 [95% CI，73.4 至 99.3 起事件]；不确定的肾素表型，53.3 个事件 [CI，42.8 至 66.4 个事件]；未抑制的肾素表型，54.5 个事件 [CI，41.8 至 71.0 个事件]）。抑制肾素时，较高的醛固酮浓度与高血压发生风险增加独立相关，而当肾素未抑制时，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，但仅限于肾素受到抑制时。

钠和钾的测量比肾素和醛固酮的测量早几年。

肾素抑制和肾素抑制背景下醛固酮浓度升高与高血压风险增加相关，也可能与 MR 活性增加相关。这些发现表明正常血压下亚临床原发性醛固酮增多症（肾素非依赖性醛固酮增多症）具有临床相关性。

美国国立卫生研究院。