Renal physiology of nocturia

Abstract

Renal function, diurnal fluctuations in arginine vasopressin (AVP) secretion, sex, and advanced age affect urine formation and may contribute to nocturia. Renal effects of AVP are mediated by AVP V2 receptors in the kidney collecting duct. Changes in AVP concentration have the greatest relative effects on urine volume when AVP levels are low; therefore small changes can have a large effect on renal water excretion. AVP is the major regulator of water excretion by the kidneys, and AVP levels have been shown to affect nocturnal voiding. Results of several studies show that patients with nocturia had no significant variation in plasma AVP, whereas patients without nocturia had significant diurnal variation in plasma AVP. The V2 receptor gene is located on the X chromosome, which has important sex-specific consequences. For example, mutations in the V2 gene can cause nephrogenic diabetes insipidus, predominantly in men. Age-related changes in water metabolism are associated with overall body composition, kidney, and brain. Older people generally experience decreased extracellular fluid and plasma volume, which leads to increased adverse consequences from net body water gain or loss. Renal function declines with age, and the ability to concentrate urine and conserve sodium is reduced in the elderly. Thirst perception is also decreased in the elderly, who, compared with younger people, tend to hypersecrete AVP in response to higher plasma osmolality, possibly resulting in hyponatremia. These aspects of renal physiology should be considered when antidiuretic drugs are prescribed for the treatment of nocturia.

Nocturia through the menopausal transition and beyond: a narrative review

“…Antidiuretic hormone (ADH) is central to the physiological regulation of free water [29]. In healthy adults, secretion of ADH by the posterior pituitary gland of the hypothalamus follows a well-defined circadian rhythm and characteristically increases across the nocturnal period, promoting the conservation of solute-free water and thus an attenuation of nocturnal diuresis [30].…”

“…In healthy adults, secretion of ADH by the posterior pituitary gland of the hypothalamus follows a well-defined circadian rhythm and characteristically increases across the nocturnal period, promoting the conservation of solute-free water and thus an attenuation of nocturnal diuresis [30]. Accordingly, excess water diuresis can be caused through an impaired secretion or activity of endogenous ADH [29]. Current evidence suggests ADH release to be sex hormone-dependent, as estrogen receptors have been found in the pituitary gland of the hypothalamus, and estrogen may also directly modulate the effects of ADH at the level of the kidney [31].…”

Pharmacotherapy for Nocturia

“…Women appear to be more sensitive to desmopressin than men. This has been attributed to the fact that the gene for the vasopressin V2 receptor is located on the X chromosome in a region with high probability of escape from inactivation; this may lead to phenotypic sex differences, with females expressing higher levels of transcript than males [ 14 , 15 ]. The lowest therapeutically beneficial dose of desmopressin (orally disintegrating tablet) has been determined as 50 μg for men [ 16 ] and 25 μg for women [ 17 ].…”

Nocturia

“…Az AVP kötődésekor megnyílnak az aquaporin 3 és 4 csatornák, amelyeken keresztül víz szí-vódik vissza a véráramba a sejtekből, míg oda az aquaporin 2 csatornán jut el a folyadék a gyűjtőcsatornából. A víz transzportját az ozmotikus nyomásgradiens vezérli [22,23].…”

“…Kísérletekkel igazolták, hogy az enuresis nocturnában szenvedőknél az éjszakai AVP-termelés csak mintegy két és félszerese a nappali szintnek. Ezzel szemben éjszakai polyuriában nem látható fokozott AVP-kiválasztás vagy éppen cirkadián ritmusának felborulása észlelhető például intracranialis folyamat miatt, mint: Parkinson-kór, sclerosis multiplex, központi idegrendszeri laesiók, térfoglalások vagy vascularis esemé-nyek [2,22,23].…”