Key result
Sodium-retention therapies like MRAs provide superior blood pressure lowering over vasoconstriction inhibitors in low-renin hypertension.
Why the study?
Expanded screening has revealed many individuals with suppressed renin who do not meet criteria for aldosterone excess, renewing interest in renin-guided therapy.
Do therapies targeting sodium retention improve blood pressure control and reduce cardiovascular risk in patients with low-renin hypertension compared to agents directed at vasoconstriction?
Do therapies targeting sodium retention improve blood pressure control and reduce cardiovascular risk in patients with low-renin hypertension compared to agents directed at vasoconstriction?
Recognizing low-renin hypertension as a distinct phenotype enables mechanism-based therapy with sodium-targeting agents, which may improve blood pressure control and mitigate long-term cardiovascular risk.
Low-renin hypertension may warrant mineralocorticoid-focused evaluation beyond aldosteronism screening; leaves open optimal diagnostics and therapies.
Low-renin hypertension is increasingly recognized as a common and clinically important form of hypertension. Expanded screening for primary aldosteronism has revealed many individuals with suppressed renin who do not meet the diagnostic criteria for aldosterone excess, yet exhibit features consistent with sodium retention or increased mineralocorticoid activity. This review synthesizes evidence from targeted literature searches on the epidemiology, mechanisms, diagnostic challenges, and treatment of low-renin hypertension. Early studies proposed renin, in the presence of hypertension, as a marker of excess sodium retention and volume expansion, suggesting that renin could guide individualized therapy. Adoption of a renin-guided treatment approach was historically limited by assay variability and concerns regarding adverse effects from high-dose mineralocorticoid receptor antagonists. However, improvements in renin assay performance, increased accessibility and use of renin testing, and the availability of lower-dose and better-tolerated mineralocorticoid receptor antagonists have renewed interest in this strategy. Low-renin hypertension encompasses primary aldosteronism, conditions that mimic mineralocorticoid excess, and disorders of renal tubular sodium transport. Across this spectrum, patients respond more favorably to therapies targeting sodium retention: mineralocorticoid receptor antagonists, epithelial sodium channel inhibitors, or thiazide diuretics, than to agents directed primarily at vasoconstriction. Recognition of low-renin hypertension as a distinct phenotype enables mechanism-based therapy and may improve blood pressure control, reduce medication burden, and mitigate long-term cardiovascular risk.
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Shah et al. (2026) conducted a review in Low-renin hypertension. Therapies targeting sodium retention (e.g., mineralocorticoid receptor antagonists) vs. Agents directed primarily at vasoconstriction was evaluated. Therapies targeting sodium retention, such as mineralocorticoid receptor antagonists, provide more favorable responses in low-renin hypertension than agents directed primarily at vasoconstriction.
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