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Relief of Nocturnal Enuresis by Desmopressin Is Kidney and Vasopressin Type 2 Receptor Independent

Joris H. Robben^*, Mozes Sze^*, Nine V. Knoers, Paul Eggert, Peter Deen^* and Dominik Müller

^* Department of Physiology, Nijmegen Centre of Molecular Life Sciences, and Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands; and University Children's Hospital, Kiel, and Department of Pediatric Nephrology, Charité Berlin, Berlin, Germany

Address correspondence to: Dr. Dominik Müller, Charité Department of Pediatric Nephrology, Augustenburger Platz 1, 13535 Berlin, Germany. Phone +49-30-450-616147; Fax +49-30-450-516912; E-mail: dominik.mueller{at}charite.de

Received for publication August 26, 2006. Accepted for publication February 11, 2007.

Primary nocturnal enuresis (PNE) is a common problem in childhood and adolescence. Although various treatments are highly effective, a common underlying hypothesis on the pathogenesis is lacking. The success of desmopressin, a synthetic analogue of the antidiuretic hormone vasopressin, has been attributed to increased renal water reabsorption that is mediated by activation of the renal vasopressin V2 receptor (V2R). However, this effect does not explain other symptoms of PNE, such as the failure to arouse upon bladder distension. This study identified a family in which one child displayed PNE and coexisting nephrogenic diabetes insipidus, as a result of a novel nonsense mutation in the V2R gene (C358X). Cell-biologic investigations revealed that V2R-C358X is retained in the endoplasmic reticulum and is unstable, which explains his nephrogenic diabetes insipidus. Consistently, extrarenal V2R-mediated responses were absent in the patient who was treated with desmopressin. Administration of desmopressin, however, changed his PNE into nocturia, because he now still voided unchanged high urinary volumes at night but woke up and went to the bathroom. Withdrawal of desmopressin was accompanied by bedwetting, whereas reintroduction again relieved the symptoms. Therefore, these data indicate that neither a functioning renal concentration system nor a functional V2R is needed for the therapeutic benefit of desmopressin in PNE. Rather, it suggests that another vasopressin receptor and other organ(s) is the target for desmopressin to relieve PNE.

This article has been cited by other articles:

				A. L. Friedman Desmopressin for Enuresis May Act on Brain Rather Than Kidney AAP Grand Rounds, September 1, 2007; 18(3): 29 - 29. [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673