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Relationship of circadian pattern of urine sodium excretion to hypertension and obstructive sleep apnoea

By L.H. White, T.D. Bradley, and A.G. Logan.

Journal of Hypertension, Volume 32, Issue 11, 2014, Pages 2253-2260

Editorial comment
It is known that nocturia is a common complaint in patients affected by obstructive sleep apnoea (OSA) and hypertension, two conditions which could be related to increased night-time sodium excretion. What is not known is whether OSA independently leads to increased night-time sodium excretion or whether it is mediated via elevated blood pressure. In this article the authors investigate the relative contributions of hypertension and OSA to disturbances of circadian sodium and water excretion as well as nocturia.

Twenty-six hypertensive patients with or without OSA and 26 normotensive patients (with and without OSA) were prospectively included in the study. All patients underwent overnight polysomnography to detect the presence or absence of OSA, 24 hour urine collection, divided into day and night samples, and continuous monitoring of bladder pressure. As a result, it was observed that, in normotensive patients, OSA had no influence on night-time urine excretion, while in hypertensive patients, OSA increased the reversal of the normal circadian sodium excretion pattern by elevating night-time urine excretion. In addition, frequency of nocturia was closely related to night-time urine excretion and blood pressure and was higher in hypertensive patients with OSA, compared to both the normotensive non-OSA and normotensive OSA groups. The present article is the first one to prospectively and objectively assess nocturia frequency, taking into account both hypertension and OSA in the analysis. These results imply that, in these patients, the reduction in nocturia frequency can be obtained by treatments addressed to control both OSA and hypertension.


Objectives: Obstructive sleep apnoea (OSA) and hypertension frequently coexist, and both are associated with higher night-time than daytime urine sodium excretion rate (UNaV). However, the relative contribution of each condition is unknown. We compared the circadian pattern of UNaV in hypertensive and normotensive patients with and without OSA.

Methods: Hypertensive [blood pressure (BP) >140/90 or on antihypertensive medications, excluding diuretics] and normotensive (BP <135/85) patients underwent overnight polysomnography to determine the presence or absence of OSA (apnoea–hypopnoea index ≥10 or <10, respectively), same-day 24-h urine collection divided into day and night-time samples and automated evening BP measurement.

Results: Twenty-six hypertensive (9 without and 17 with OSA) and 26 normotensive (15 without and 11 with OSA) patients were studied. Night-time UNaV was higher in the hypertensive than the normotensive patients. Whereas in the normotensive patients night-time UNaV was unaffected by OSA, in the hypertensive patients, it was higher in those with than without OSA (P = 0.009 for OSA × hypertension interaction). Night : day UNaV ratio was higher in hypertensive than normotensive patients, but was not significantly affected by OSA in either group. On multivariate analysis, SBP and apnoea–hypopnoea index were independent predictors of night-time UNaV (model r2 = 0.574, P < 0.001) and night : day UNaV ratio (model r2 = 0.397, P < 0.001). However, SBP was the strongest independent predictor.

Conclusions: In hypertensive patients, OSA exacerbates the reversal of the normal circadian sodium excretion pattern by elevating nocturnal UNaV, possibly via its BP-elevating effects. However, OSA does not affect nocturnal UNaV in normotensive patients.