Over 80% of individuals with obesity-related hypertension exhibited pathologic phenotypes of aldosteronism and/or hypercortisolism, supporting targeted hormonal therapies.
The high prevalence of overlapping aldosteronism and hypercortisolism phenotypes in patients with obesity-related hypertension provides mechanistic support for targeted aldosterone- and cortisol-directed therapies.
Understanding hormonal mechanisms of obesity-related hypertension may inform targeted therapy. Participants with obesity and hypertension underwent deep-phenotyping procedures to detect the primary aldosteronism phenotype, low-renin phenotype, renin-dependent aldosteronism phenotype, and ACTH-independent hypercortisolism. In total, 51.9% of participants had a primary aldosteronism phenotype, of which approximately one-half also had superimposed renin-dependent aldosteronism. Another 23.4% of participants had only renin-dependent aldosteronism that was characterized by higher aldosterone levels and kaliuresis, and 9.2% of participants also had hypercortisolism. Over 80% of individuals with obesity-related hypertension exhibited overlapping pathologic phenotypes of aldosteronism and/or hypercortisolism, providing mechanistic evidence to support the efficacy of aldosterone- and cortisol-directed therapy.
Salle et al. (2026) studied this question. Over 80% of individuals with obesity-related hypertension exhibited pathologic phenotypes of aldosteronism and/or hypercortisolism, supporting targeted hormonal therapies.