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Aim: To detect effects of desmopressin on sleep in enuretic children and to look for polysomnographical differences between responders and non-responders to desmopressin treatment.Methods: Twenty-one children with primary nocturnal enuresis were examined polysomnographically before treatment. All but one of the children then received treatment with desmopressin in standard dosage, and the response was documented. Seven of the children underwent a second polysomnographic registration while on treatment.Results: The time interval (+/- 1 SD) between sleep onset and the enuretic episode was 92 +/- 67 min without medication and 372 +/- 157 min when desmopressin was given (p = 0.003). Standard polysomnographic variables were not affected by the drug. Ten children were desmopressin responders and 10 were non-responders. The total sleep time was 455 +/- 56 min in the former and 408 +/- 31 min in the latter group (p = 0.04). The responders spent 27.4 +/- 5.5% of their total sleep time in rapid eye movement sleep, compared with 18.2 +/- 6.5% in the non-responder group (p = 0.004).Conclusion: Desmopressin has no major effects on sleep as such but does delay bladder emptying. Enuretic children responding to desmopressin treatment have more rapid eye movement sleep than therapy-resistant children. [ABSTRACT FROM AUTHOR]

Objective To test the hypotheses that vasopressin deficiency or hypercalciuria are important in polyuric and non-polyuric bedwetting, as nocturnal polyuria is a pathogenetic factor in enuresis responsive to antidiuretic therapy with desmopressin. Subjects and methods Vasopressin deficiency has been implicated as a cause of nocturnal polyuria, but measurements of vasopressin in plasma have given contradictory results, because the hormone is released in pulses. Urinary levels reflect the secretion over longer periods. Hypercalciuria has also been proposed as a pathogenetic factor. Twenty-eight enuretic children who responded to desmopressin therapy with or without added anticholinergic agents (diuresis-dependent enuresis, DE), 15 children with therapy-resistant enuresis (not diuresis-dependent, NDE) and 51 continent controls were assessed. Urinary vasopressin, calcium and osmolality were measured in the morning after a 12-h thirst provocation. Urine production was recorded for 2 days. Results Because most data were not normally distributed, the values are expressed as the median (range). There were no differences in urine osmolality; i.e. con-trols 919 (636–1232), DE 849 (462–1149), NDE 968 (664–1191) mOsml/kg); vasopressin, controls 34 (8–983), DE 26 (9–295), NDE 50 (9–116) pmol/L; or calcium excretion (expressed as the calcium/creatinine ratio), controls 0.16 (0.01–0.71), DE 0.14 (0.04–0.67), and NDE 0.23 (0.03–0.69). The DE group produced more urine, at 18.4 (9.2–52.5) mL/kg/day, than the other groups, i.e. control 12.7 (8.3–42.8) and NDE 12.1 (6.3–36.8) mL/kg/day (P = 0.008). Conclusion All enuretic children with nocturnal polyuria do not have vasopressin deficiency. The urinary calcium excretion does not differ between enuretic and dry children. [ABSTRACT FROM AUTHOR]

Compares desmopressin responders and non-responders with respect to pharmacokinetics and renal effects of desmopressin. Absence of pharmacokinetic differences between the groups; Smaller spontaneous bladder capacity of non-responders; Less concentrated urine produced by responders; Urodynamic defect among non-responders; Osmoregulatory defect among responders.