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Primary aldosteronism (PA) is an endocrine disorder that results from aldosterone overproduction by the adrenal glands, independent of physiological stimuli (hyperkalemia or renin). Symptomatic PA can cause hypertension and hypokalemia, but PA exists across a spectrum of severity from subclinical disease to treatment-resistant hypertension and from normokalemia to severe hypokalemia. PA remains underdiagnosed despite the fact that targeted therapies can reduce morbidity and mortality.1,2 This Clinical Insights article provides clinicians with a practical approach to diagnosing and managing PA.
Hypertension is the leading modifiable risk factor worldwide for ASCVD, and approximately half of US adults have hypertension.1 Uncontrolled BP contributes to heart failure, stroke, atrial fibrillation, and sudden cardiac death and is associated with development of kidney failure and dementia.2 This guideline was designed to provide clinicians with a risk stratification approach to managing BP. This synopsis highlights key guideline recommendations.
Primary aldosteronism (PA) is common among patients with hypokalemia and hypertension. Patients with PA are at an increased risk of chronic disease if undiagnosed or untreated. Expert consensus recommends screening for PA in high-risk populations. Most antihypertensive medications can be continued during the work-up for PA. An elevated aldosterone-to-renin ratio is suggestive of PA.
Primary aldosteronism is a nonsuppressible renin-independent aldosterone production that causes hypertension and cardiovascular disease.
Objective:
To characterize the prevalence of nonsuppressible renin-independent aldosterone production, as well as biochemically overt primary aldosteronism, in relation to blood pressure.
Participants completed an oral sodium suppression test, regardless of aldosterone or renin levels, as a confirmatory diagnostic for primary aldosteronism and to quantify the magnitude of renin-independent aldosterone production. Urinary aldosterone was measured in participants in high sodium balance with suppressed renin activity. Biochemically overt primary aldosteronism was diagnosed when urinary aldosterone levels were higher than 12 µg/24 h.
Results:
Every blood pressure category had a continuum of renin-independent aldosterone production, where greater severity of production was associated with higher blood pressure, kaliuresis, and lower serum potassium levels. Mean adjusted levels of urinary aldosterone were 6.5 µg/24 h (95% CI, 5.2 to 7.7 µg/24 h) in normotension, 7.3 µg/24 h (CI, 5.6 to 8.9 µg/24 h) in stage 1 hypertension, 9.5 µg/24 h (CI, 8.2 to 10.8 µg/24 h) in stage 2 hypertension, and 14.6 µg/24 h (CI, 12.9 to 16.2 µg/24 h) in resistant hypertension; corresponding adjusted prevalence estimates for biochemically overt primary aldosteronism were 11.3% (CI, 5.9% to 16.8%), 15.7% (CI, 8.6% to 22.9%), 21.6% (CI, 16.1% to 27.0%), and 22.0% (CI, 17.2% to 26.8%). The aldosterone–renin ratio had poor sensitivity and negative predictive value for detecting biochemically overt primary aldosteronism.
Limitation:
Prevalence estimates rely on arbitrary and conventional thresholds, and the study population may not represent nationwide demographics.
Conclusion:
The prevalence of primary aldosteronism is high and largely unrecognized. Beyond this categorical definition of primary aldosteronism, there is a prevalent continuum of renin-independent aldosterone production that parallels the severity of hypertension. These findings redefine the primary aldosteronism syndrome and implicate it in the pathogenesis of “essential” hypertension.
