Primary aldosteronism and obstructive sleep apnea in hypertension: interplay, target organ damage, and clinical management.

Primary aldosteronism (PA) and obstructive sleep apnea (OSA) are common but often unrecognized contributors to hypertension. When they coexist, aldosterone excess, fluid redistribution, intermittent hypoxia, sympathetic activation, and shared metabolic risk may increase hypertension-mediated organ damage. This narrative review examines the evidence linking PA and OSA, with emphasis on mechanisms, cardiovascular and renal consequences, diagnostic limitations, and clinical management. Aldosterone-related sodium retention and nocturnal rostral fluid shift may worsen upper-airway obstruction. Conversely, intermittent hypoxia, sleep fragmentation, and sympathetic activation in OSA may alter renin-angiotensin-aldosterone system activity, although OSA does not account for autonomous aldosterone secretion. Both disorders are associated with oxidative stress, inflammation, endothelial dysfunction, cardiac remodeling, and renal injury. Their overlap should be considered in patients with resistant hypertension, hypokalemia, adrenal incidentaloma, clinically suspected OSA, or organ damage not fully explained by measured blood pressure. Management requires independent confirmation of each disorder, subtype-directed PA treatment with adrenalectomy or mineralocorticoid receptor antagonists, and appropriate OSA treatment with positive airway pressure or other individualized measures. Multidisciplinary care may improve blood pressure and intermediate organ outcomes, but prospective studies are needed to determine whether combined treatment reduces long-term cardiovascular, renal, and cerebrovascular events.