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Vasopressin and hypercalciuria in enuresis: a reappraisal

Nevéus T, Hansell P, Stenberg A

BJU international, 2002

15 participants

Abstract

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)…

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Evidence Hub reads this as a clinical trial, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 15 participants or records.

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