Vasopressin and hypercalciuria in enuresis: a reappraisal

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.