Condition may be due largely to abnormal nocturnal renal handing of solutes, especially sodium.
Children with a form of nocturnal enuresis that does not respond to therapy may have more sodium and urea in their nighttime urine, possibly because of an imbalance of prostaglandin, according to a new study by Danish researchers.
They say their findings may help explain why about 30% of children who suffer from nocturnal enuresis do not respond to desmopressin, which successfully treats the other 70%. The findings appear in the American Journal of Physiology-Renal Physiology (2006;291:F1232-F1240).
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The researchers, from the University of Aarhus, noted that urine output is controlled, in part, by circadian rhythms. With the transition from day to night, there is a reduction in the amount of excreted water, electrolytes and other metabolic end products in preparation for hours of sleep. It is believed that a person is not born with this circadian rhythm, but it usually develops in early childhood.
The researchers report that some children take longer to develop this rhythm, which is why about 15% of enuretic children will spontaneously stop bedwetting each year without any intervention.
The investigators examined 46 enuretic children (aged 7-14 years) who were outpatients at the Center for Child Incontinence at Aarhus University Hospital and whose enuresis had failed to respond to desmopressin. The enuretic children were subdivided into a polyuric group (average nocturnal output on wet nights exceeded 130% of expected bladder capacity) and a nonpolyuric group (output on wet nights less than 130% of expected capacity). The study also included an age-matched control of 15 non-enuretic children.
All children spent two nights at the university hospital. The first night was to acclimate the children to the environment, and the second night was the experimental period. Blood and urine were collected during the second night, without waking the subjects.
This gave a more complete picture of physiological changes that occur through the course of an entire night. Fluid and sodium intake was standardized for all children, based on their weight, to eliminate the possibility that enuretic episodes were related either to excess sodium or fluid intake. All children had adequate bladder capacity and were healthy. None experienced daytime incontinence.
Circadian variations in urine output were evident for all groups. However, polyuric children excreted twice as much urine during the night compared to the nonpolyuric children and the controls. The urine of the polyuric children who wet their beds during the experiment contained more sodium, urea, and prostaglandin. Some enuretic children (five polyurics and four nonpolyurics) did not have a wet night during their hospital stay.
The children who wet the bed did not excrete a greater volume of water, but the sodium and urea content of their urine was higher. These substances expand the volume of urine in the bladder, leading to enuresis. Additionally, urine from enuretic episodes in the first hours of sleep was different from the urine collected in the morning.
“When we look at what happens in the last hours of the night, we couldn’t find any differences,” said investigator Konstan-tinos Kamperis, MD. “The first hours are most important.”
The doctors looked at a variety of other factors that could play a role in bedwetting, including mean arterial pressure, heart rate, atrial natriuretic peptide, angiotensin II, aldosterone and renin levels, but found no differences among the groups. In addition, there were no differences in the amounts of vasopressin between the two enuretic groups. “We found enuresis-related polyuria to be largely due to an abnormal nocturnal renal handling of solutes and in particular, sodium,” the authors wrote.
