Nocturnal polyuria in monosymptomatic nocturnal enuresis refractory to desmopressin treatment

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.

The Prevalence of Nocturia and Nocturnal Polyuria After Renal Transplantation and Associated Factors

“…Nocturia and nocturnal polyuria are symptoms of a variety of pathological conditions, including DM (24), cardiovascular diseases (25), renal diseases (26,27), and enuresis (28). It seems that different pathological mechanisms are responsible for abnormal circadian rhythm in diuresis (11).…”

“…It seems that different pathological mechanisms are responsible for abnormal circadian rhythm in diuresis (11). In children with enuresis, lack of a nocturnal increase in arginine vasopressin (AVP) level, disorders in hormones regulating renal sodium (aldosterone and angiotensin II), and overproduction of prostaglandin E2 (PGE2) have been reported (28)(29)(30)(31). The overnight decrease in blood pressure leads to an increase in AVP (32).…”

Nocturnal enuresis

“…Excessive nocturnal urine production in some children is based on abnormal nocturnal plasma vasopressin release. 6,7 Other children may have an "overactive bladder;" however, these children typically have daytime symptoms including urgency, frequency and incontinence. Yeung performed ambulatory cystometries and found that bladder overactivity is an important cause of therapyresistant nocturnal enuresis.…”

The effect of familial aggregation on the children with primary nocturnal enuresis

“…If an average NUO on wet nights exceeded 130% of the expected bladder capacity for age (EBCFA), the child was defined as having nocturnal polyuria. 13 MVV was estimated as the maximal voided volume observed (morning void included), and the children with MVV less than 70% of EBCFA were considered to have a small bladder. 14 Daytime urodynamic studies were performed in all patients using DUET Logic urodynamic unit (Medtronic Corporation, Denmark) according to the recommendations of ICCS.…”