Nocturnal enuresis is caused by a mismatch between nocturnal diuresis and functional bladder volume. Increased nocturnal diuresis is classically described in monosymptomatic nocturnal enuresis (without bladder dysfunction = LUTS) and attributed to abnormal circadian rhythm of vasopressin: low nocturnal vasopressin levels result in high diuresis and low urinary osmolality, and by definition a good response to desmopressin (Rittig et al. ). But only 30% of patients with nocturnal polyuria are full responders to desmopressin, suggesting that nocturnal polyuria is more than increased water diuresis. Kamperis et al (Am J Physiol Renal Physiol 2006, J Urol. 2004), Vande Walle et al (J Urol. 2007) and Raes et al (J Urol. 2006) documented in pilot studies that desmopressin resistance correlates with abnormal circadian rhythms of different renal functions (glomerular (GFR) and tubular (water, solute and salt excretion)). These findings are very similar to what Goessaert and Everaert found in adults with nocturia. They documented that not only the increased water but also the high solute excretion os mainly present early in the night. In addition, nocturnal polyuria occurs not only in monosymptomatic (MNE) but also in non-monosymptomatic (NMNE), something that has been inadequately studied in the literature and most of these studies were conducted using the old NMNE/MNE definitions and not the new ones.
The aim of this study is to document the incidence, severity and timing of nocturnal polyuria and to analyze the circadian rhythm of GFR, water diuresis, and salt and osmotic excretion. And this both in children with MNE and NMNE (where we will use the different definitions).
Study population is a large anonymized database of children with enuresis, in which a standardized screening was done at inclusion: Standardized enuresis history, clinical examination CMT, ultrasound, uroflow and 24h urine concentration profile validated. All this data was processed in a large, fully anonymized database