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NDT Advance Access originally published online on March 29, 2007
Nephrology Dialysis Transplantation 2007 22(7):1853-1855; doi:10.1093/ndt/gfm136
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

V2-antagonists for the treatment of hyponatraemia*

Guy Decaux

Department of General Internal Medicine, Erasme University Hospital, Brussels, Belgium

Correspondence and offprint requests to: Guy Decaux, Department of General Internal Medicine, Erasme University Hospital, Brussels, Belgium. Email: guy.decaux@skynet.be

Keywords: hyponatraemia; vasopressin; V2-receptor antagonist

The first 10% of the full text of this article appears below.

Hypotonic hyponatraemia results from an excess of total body water relative to the exchangeable sodium and potassium pool due to a decrease in electrolyte-free water (EFWC) excretion [1]. The decrease in free water excretion is mostly due to the secretion of the antidiuretic hormone (ADH), also called vasopressin. This secretion is either ‘appropriate’ when it is a result of volume stimuli, or ‘inappropriate’, as in the syndrome of inappropriate secretion of ADH (SIADH), when osmotic or volume stimuli are lacking. Vasopressin is involved in most cases of sustained hyponatraemia. Therefore, the use of specific blockers of vasopressin receptors is a logical approach in the treatment of patients with SIADH or hypervolemic hyponatraemia and may offer . . . [Full Text of this Article]


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