ArticleSleep & breathing = Schlaf & Atmung2026
Dissociation between nocturnal hypoxemic burden and renin suppression: evidence of sympathetic activation in primary aldosteronism.
Article in Sleep & breathing = Schlaf & Atmung, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposePrimary aldosteronism (PA) is frequently accompanied by sleep-disordered breathing, yet the physiological consequences of nocturnal hypoxemia in this population remain poorly understood. Although intermittent hypoxemia is known to activate both the sympathetic nervous system and the renin-angiotensin-aldosterone system in obstructive sleep apnea, whether these responses are preserved in PA, where plasma renin activity (PRA) is chronically suppressed, remains unclear. We investigated the associations between nocturnal hypoxemic burden and autonomic, hormonal, and cardiac markers in patients with PA.
methodsFifty consecutive patients with PA underwent overnight portable sleep monitoring. Nocturnal hypoxemia was assessed using the 3% oxygen desaturation index (ODI), time spent with oxygen saturation below 90% (T90), and minimum oxygen saturation. Pulse rate surges were used as surrogate markers of autonomic activation. Associations between nocturnal hypoxemia and pulse rate surges, PRA, and B-type natriuretic peptide (BNP) were evaluated using Spearman's correlation and multivariable linear regression analyses adjusted for age, body mass index, and PA subtype.
resultsT90 showed no significant association with PRA (ρ = 0.021, p = 0.883) or BNP (ρ = - 0.150, p = 0.307). In contrast, T90 was independently associated with pulse rate surges after multivariable adjustment (β = 0.468, p < 0.001). Although ODI correlated with pulse rate surges in univariable analysis, it was not independently associated after adjustment, whereas T90 remained significant.
conclusionsNocturnal hypoxemic burden was independently associated with autonomic activation but not with renin activity or cardiac stress in patients with PA. These findings suggest that hypoxemia-driven sympathetic activation occurs independently of renin suppression, indicating a physiological dissociation between neural and hormonal responses in PA. Assessment of hypoxemic burden may therefore provide clinically relevant information beyond conventional measures of sleep-disordered breathing.
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