Effect of DDAVP on Nocturnal Enuresis in a Patient with Nephrogenic Diabetes Insipidus
| Title: | Effect of DDAVP on Nocturnal Enuresis in a Patient with Nephrogenic Diabetes Insipidus |
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| Authors: | Jonat, Susanne; Santer, Rene; Schneppenheim, Reinhard; Obser, Tobias; Eggert, Paul |
| Publisher: | Archives of Disease in Childhood |
| Date Published: | July 01, 1999 |
| Reference Number: | 479 |
The case of an 8 year old boy with both nocturnal enuresis and nephrogenic diabetes insipidus is presented. Diagnosis of nephrogenic diabetes insipidus was based on a typical medical history, the characteristic result of a fluid restriction test, the lack of an effect of 1-desamino-8-D-arginine (DDAVP) on both urine osmolality and plasma coagulation factors and, finally, the detection of a hemizygous missense mutation within the arginine vasopressin (AVP) receptor gene. Hydrochlorothiazide treatment and dietary measures reduced the patient's urine volume to one third of its original volume. However, this had no effect on enuresis. The daily intranasal application of DDAVP did not further reduce urine output but dramatically decreased the frequency of bed wetting. This observation contradicts the common notion that the therapeutic effect of DDAVP in nocturnal enuresis is the result of compensation for a nocturnal AVP deficit. Rather, it points to a different mode of action of DDAVP in patients with enuresis. It is hypothesised that central AVP receptors are a target of DDAVP and that they might play an important role in the pathogenesis of nocturnal enuresis.
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This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
Jonat, et al., present the case of an 8-year-old boy who had both XNDI and nocturnal enuresis (involuntary bed-wetting at night). After diagnosing the boy's XNDI, the authors prescribed a standard treatment regime: daily administration of hydrochlorothiazide along with a salt restricted, low protein diet. This reduced the boy's fluid intake and reduced his urine volume to one-third of its original volume. However, this treatment had no effect on his nocturnal enuresis, which continued to occur 5-6 nights per week. So the authors prescribed nightly applications of dDAVP, a standard treatment for nocturnal enuresis. This had no effect on the patient's urine volume output or fluid intake (remember, the patient's vasopressin-2 receptors could not bind with AVP or dDAVP), but it did reduce the incidence of bedwetting to 2-3 nights per month.
The medical community prescribes dDAVP for children with nocturnal enuresis on the hypothesis that their AVP secretion is insufficient at night, resulting in increased urine, which exceeds bladder capacity. Yet this hypothesis is contested and unproven. The authors' case provides additional evidence against it. The authors speculate that patients with nocturnal enuresis do not have insufficient amounts of AVP; instead, they have a defect at the AVP receptor level. It could not be the V2Rs because their patient had XNDI, which means he had defective V2Rs incapable of binding with AVP or dDAVP. Thus, applications of dDAVP would have no effect on nocturnal enuresis if the dDAVP had to bind with V2R in order to exert its effect.
The authors speculate that another AVP receptor, AVPR3 (also called AVPR1b) is a target of dDAVP in children with enuresis. Jonat, et al., speculate that AVPR3s play a role in the central nervous regulation of bladder control and that they may play an important role in the development of nocturnal enuresis.