RENAL SODIUM HANDLING ABNORMALITY IN OBSTRUCTIVE SLEEP APNEA-RELATED HYPERTENSION

Abstract

Objective: Obstructive sleep apnea (OSA) has been much focused as one of underlying factors of resistant hypertension. A substantial number of mechanisms (sympathetic nerve activation, oxidative stress, renin-angiotensin-aldosterone system, systemic inflammation and fluid retention) contributed to OSA-related hypertension, and these factors can lead to resistant hypertension. However, renal sodium handling abnormality in OSA patients with hypertension has not been fully clarified. Design and method: We evaluated the urine sodium excretion before and after continuous positive airway pressure (CPAP) therapy in OSA. 24-h urinary sodium excretion was estimated at baseline and after 6 months of CPAP using the Kawasaki formula, and fractional urinary sodium excretion (FENa) was also calculated in 23 OSA patients with hypertension. Results: In patients with severe OSA, 24 h Na excretion had no significant correlation with AHI, abdominal circumference and plasma aldosterone. After CPAP therapy, systolic blood pressure significantly decreased (P < 0.05), and estimated sodium excretion significantly increased compared to baseline (P < 0.05). The increase in Na excretion was significantly associated with BP reduction by CPAP therapy. Conclusions: These results suggested that urine sodium excretion abnormality contribute to the blood pressure elevation in patients with OSA. Therefore, urine sodium excretion may be a key mechanism in managing OSA-related hypertension.