Excess diuresis and natriuresis during acute sleep deprivation in healthy adults

Abstract

The transition from wakefulness to sleep is associated with a pronounced decline in diuresis, a necessary physiological process that allows uninterrupted sleep. The aim of this study was to assess the effect of acute sleep deprivation (SD) on urine output and renal water, sodium, and solute handling in healthy young volunteers. Twenty young adults (10 male) were recruited for two 24-h studies under standardized dietary conditions. During one of the two admissions, subjects were deprived of sleep. Urine output, electrolyte excretions, and osmolar excretions were calculated. Activated renin, angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide were measured in plasma, whereas prostaglandin E(2) and melatonin were measured in urine. SD markedly increased the diuresis and led to excess renal sodium excretion. The effect was more pronounced in men who shared significantly higher diuresis levels during SD compared with women. Renal water handling and arginine vasopressin levels remained unaltered during SD, but the circadian rhythm of the hormones of the renin-angiotensin-aldosterone system was significantly affected. Urinary melatonin and prostaglandin E(2) excretion levels were comparable between SD and baseline night. Hemodynamic changes were characterized by the attenuation of nocturnal blood pressure dipping and an increase in creatinine clearance. Acute deprivation of sleep induces natriuresis and osmotic diuresis, leading to excess nocturnal urine production, especially in men. Hemodynamic changes during SD may, through renal and hormonal processes, be responsible for these observations. Sleep architecture disturbances should be considered in clinical settings with nocturnal polyuria such as enuresis in children and nocturia in adults.

Sleep Duration and Chronic Kidney Disease: Analysis of the National Health Interview Survey

“…Although the direct renal effects of aberrant sleep duration have not been extensively investigated, emerging evidence suggests that sleep deprivation could interfere with normal renal physiology. Acute sleep deprivation in humans reduces plasma renin, angiotensin, and aldosterone levels, and is associated with increased urinary excretion of sodium and potassium [20,21]. In addition, the normal nocturnal dipping of blood pressure is attenuated.…”

Correlates for nocturia: A review of epidemiological studies

“…Middelkoop et al reported that the most frequent subjective cause of disturbed sleep maintenance is nocturia (67.5%), 51 and Bliwise et al reported that nocturia is an independent predictor of selfreported insomnia and reduced sleep quality. 52 In contrast, excessive diuresis and natriuresis during the night are induced by acute sleep deprivation, as shown by Kamperis et al 102 While the cause or effect is unclear, several epidemiological studies have shown a correlation of insomnia/ poor sleep to nocturia. 14,26,76,103 As well as sleep quality, duration of sleep is associated with the number of nocturia episodes.…”

The Circadian Clock Modulates Renal Sodium Handling

“…For instance, Kamperis et al have shown that acute sleep deprivation in humans leads to excessive natriuresis and kaliuresis during the subjective night and attenuation of the nocturnal BP dip. 8 Numerous studies have demonstrated an impairment of the sodium excretory rhythm and the development of hypertension in shift workers. 9,10 The circadian clock can influence renal function via two types of circadian inputs: (1) entrainment of renal rhythms through the external circadian time cues, such as hormones, food, activity, and body temperature rhythms, and (2) the activity of the intrinsic renal circadian clock.…”