De Guchtenaere A, Vande Walle C, Van Sintjan P, Raes A, Donckerwolcke R, Van Laecke E, Hoebeke P, Vande Walle J
Paediatric Uro-nephrological Center, University Hospital Gent, Gent, Belgium.
J Urol. 2007 Dec;178(6):2626-9. doi: 10.1016/j.juro.2007.08.028. Epub 2007 Oct 22.
Monosymptomatic nocturnal enuresis is frequently associated with nocturnal polyuria and low urinary osmolality during the night. Initial studies found decreased vasopressin levels associated with low urinary osmolality overnight. Together with the documented desmopressin response, this was suggestive of a primary role for vasopressin in the pathogenesis of enuresis in the absence of bladder dysfunction. Recent studies no longer confirm this primary role of vasopressin. Other pathogenetic factors such as disordered renal sodium handling, hypercalciuria, increased prostaglandins and/or osmotic excretion might have a role. So far, little attention has been given to abnormalities in the circadian rhythm of glomerular filtration rate. We evaluated the circadian rhythm of glomerular filtration rate and diuresis in children with desmopressin resistant monosymptomatic nocturnal enuresis and nocturnal polyuria.
We evaluated 15 children (9 boys) 9 to 14 years old with monosymptomatic nocturnal enuresis and nocturnal polyuria resistant to desmopressin treatment. The control group consisted of 25 children (12 boys) 9 to 16 years old with monosymptomatic nocturnal enuresis without nocturnal polyuria.
Compared to the control population, children with nocturnal polyuria lost their circadian rhythm not only for diuresis and sodium excretion but also for glomerular filtration rate.
Patients with monosymptomatic nocturnal enuresis and nocturnal polyuria lack a normal circadian rhythm for diuresis and sodium excretion, and the circadian rhythm of glomerular filtration rate is absent. This absence of circadian rhythm of glomerular filtration rate and/or sodium handling cannot be explained by a primary role of vasopressin, but rather by a disorder in circadian rhythm of renal glomerular and/or tubular functions.
单症状性夜间遗尿常与夜间多尿及夜间低尿渗透压相关。最初的研究发现夜间抗利尿激素水平降低与夜间低尿渗透压有关。结合已记录的去氨加压素反应,这提示在无膀胱功能障碍的情况下,抗利尿激素在遗尿发病机制中起主要作用。近期研究不再证实抗利尿激素的这一主要作用。其他致病因素如肾钠处理紊乱、高钙尿症、前列腺素增加和/或渗透性排泄可能起作用。到目前为止,肾小球滤过率昼夜节律异常很少受到关注。我们评估了去氨加压素抵抗的单症状性夜间遗尿和夜间多尿患儿的肾小球滤过率和利尿的昼夜节律。
我们评估了15名9至14岁的单症状性夜间遗尿且对去氨加压素治疗抵抗的夜间多尿患儿(9名男孩)。对照组由25名9至16岁的单症状性夜间遗尿但无夜间多尿的患儿(12名男孩)组成。
与对照组相比,夜间多尿患儿不仅在利尿和钠排泄方面失去了昼夜节律,在肾小球滤过率方面也失去了昼夜节律。
单症状性夜间遗尿和夜间多尿患者在利尿和钠排泄方面缺乏正常的昼夜节律,且不存在肾小球滤过率的昼夜节律。肾小球滤过率和/或钠处理的昼夜节律缺失不能用抗利尿激素的主要作用来解释,而更可能是由肾小球和/或肾小管功能的昼夜节律紊乱所致。