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Life sciences · Journal article
Dialogues in Health · August 19, 2026
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Purpose. Hypertension-related end-organ damage disproportionately affects Black populations, with earlier onset, greater severity, and higher rates of heart failure and chronic kidney disease despite treatment. Because structural injury may persist even when blood-pressure (BP) targets are met, this review examines aldosterone-mineralocorticoid receptor (MR) signaling as a driver of residual tissue injury and develops a hypothesis-generating framework for earlier, risk-stratified MR antagonism.Methods. This is a narrative review. We searched PubMed/MEDLINE and the Cochrane Library (inception-July 2026) using terms including mineralocorticoid receptor antagonist, aldosterone, spironolactone, eplerenone, finerenone, hypertension, resistant hypertension, end-organ damage, fibrosis, hyperkalemia, chronic kidney disease, heart failure, and health disparities. We prioritized randomized controlled trials, prespecified pooled analyses, mechanistic studies, and current guidelines, and hand-searched reference lists. No quantitative synthesis was performed.Findings. Aldosterone-MR signaling promotes fibrosis, inflammation, oxidative stress, and adverse remodeling across cardiovascular and renal tissues, and may be particularly relevant in low-renin, salt-sensitive phenotypes observed more frequently, on average, among Black patients. Randomized trials support MR antagonists (MRAs) in resistant hypertension, heart failure, and diabetic CKD; however, MRAs are often introduced late, when reduced renal function raises hyperkalemia risk and limits preventive benefit.Conclusion. In selected higher-risk patients with preserved renal function and controlled potassium, earlier MR antagonism may warrant prospective evaluation as a tissue-protective, disparity-reducing strategy. This framework is hypothesis-generating and is intended to stimulate research, not to alter current guideline-directed therapy.