Key result
Primary aldosteronism is a common cause of secondary hypertension, with its prevalence increasing in parallel with hypertension severity and spanning a continuum of dysregulated aldosterone secretion.
Why the study?
Determining the precise disease burden of primary aldosteronism remains challenging due to heterogeneity in testing, arbitrary thresholds, and populations studied.
What is the prevalence of primary aldosteronism across the blood pressure spectrum and in specific high-risk subgroups?
What is the prevalence of primary aldosteronism across the blood pressure spectrum and in specific high-risk subgroups?
Primary aldosteronism is a common and modifiable cause of secondary hypertension that spans a continuum of severity, highlighting the need for broader screening beyond traditional high-risk groups.
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May warrant broader screening consideration in hypertension; leaves open optimal detection thresholds and prospective validation.
Primary aldosteronism (PA) is characterized by dysregulated, renin-independent aldosterone excess. Long perceived as rare, PA has emerged as one of the most common causes of secondary hypertension. Failure to recognize and treat PA results in cardiovascular and renal complications, through processes mediated by both direct target tissue insults and indirectly, by hypertension. PA spans a continuum of dysregulated aldosterone secretion, which is typically recognized in late stages after treatment-resistant hypertension and cardiovascular and/or renal complications develop. Determining the precise disease burden remains challenging due to heterogeneity in testing, arbitrary thresholds, and populations studied. This review summarizes the reports on PA prevalence among the general population and in specific high-risk subgroups, highlighting the impact of rigid versus permissive criteria on PA prevalence perception.
Charoensri et al. (2023) conducted a review in Primary aldosteronism. Primary aldosteronism is a common cause of secondary hypertension, with its prevalence increasing in parallel with hypertension severity and spanning a continuum of dysregulated aldosterone secretion.
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