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去氨加压素治疗无效的单纯症状性夜间遗尿症中的夜间多尿。

Nocturnal polyuria in monosymptomatic nocturnal enuresis refractory to desmopressin treatment.

作者信息

Kamperis K, Rittig S, Jørgensen K A, Djurhuus J C

机构信息

Institute of Clinical Medicine, University of Aarhus, Aarhus N, Denmark.

出版信息

Am J Physiol Renal Physiol. 2006 Dec;291(6):F1232-40. doi: 10.1152/ajprenal.00134.2006. Epub 2006 Jun 27.

DOI:10.1152/ajprenal.00134.2006
PMID:16804103
Abstract

The transition from day to night is associated with a pronounced decline in diuresis with reductions in the amount of excreted water, electrolytes, and other end products of our metabolism. Failure to do so leads to a large urine output at night, a condition known as nocturnal polyuria, encountered in a large proportion of children with nocturnal enuresis. The aim of this study was to clarify the mechanisms responsible for the nocturnal polyuria seen in enuretics with inadequate response to desmopressin (dDAVP). Forty-six enuretics (7-14 yr of age) and fifteen age-matched controls were admitted for a 24-h protocol with standardized fluid and sodium intake, comprising urine collections, blood sampling, and blood pressure monitoring. We included patients with severe enuresis (5 +/- 1 wet nights/wk) showing <50% reduction in wet nights on dDAVP. We characterized the patients on the basis of their nocturnal urine production. The children with nocturnal polyuria excreted larger amounts of sodium and urea at night than nonpolyurics and controls. Solute-free water reabsorption as well as urinary arginine vasopressin and aquaporin-2 excretion were normal in polyurics, and no differences were found in atrial natriuretic peptide, angiotensin II, aldosterone, and renin levels. Urinary prostaglandin E2 (PGE2) excretion was significantly higher in polyurics. The nocturnal polyuria in children with dDAVP-resistant nocturnal enuresis seems to be the result of augmented sodium and urea excretion. The high urinary PGE2 levels found in these children point toward a role for increased prostaglandin synthesis in the pathogenesis of enuresis-related polyuria.

摘要

从白天到夜晚的转变与利尿作用显著下降相关,同时排出的水分、电解质及其他代谢终产物的量也会减少。若未能如此,则会导致夜间尿量增多,即所谓的夜间多尿症,这在很大一部分夜间遗尿症儿童中较为常见。本研究的目的是阐明对去氨加压素(dDAVP)反应欠佳的遗尿症患者出现夜间多尿的机制。46名遗尿症患者(7至14岁)和15名年龄匹配的对照组人员接受了一项为期24小时的方案,其中包括标准化的液体和钠摄入,涵盖尿液收集、血液采样及血压监测。我们纳入了重度遗尿症患者(每周尿床5±1次),这些患者在使用dDAVP后尿床次数减少不到50%。我们根据患者的夜间尿量对其进行了特征描述。夜间多尿的儿童夜间排出的钠和尿素量比非多尿症儿童及对照组更多。多尿症患者的无溶质水重吸收以及尿精氨酸加压素和水通道蛋白-2的排泄均正常,且在心房利钠肽、血管紧张素II、醛固酮和肾素水平方面未发现差异。多尿症患者的尿前列腺素E2(PGE2)排泄显著更高。对dDAVP耐药的夜间遗尿症儿童的夜间多尿似乎是钠和尿素排泄增加的结果。这些儿童中发现的高尿PGE2水平表明前列腺素合成增加在遗尿症相关多尿症的发病机制中起作用。

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