title: [Hormonal dysnatremia].
abstract: Because of antidiuretic hormone (ADH) disorder on production or function we can observe dysnatremia. In the absence of production by posterior pituitary, central diabetes insipidus (DI) occurs with hypernatremia. There are hereditary autosomal dominant, autosomal recessive or X- linked forms. When ADH is secreted but there is an alteration on his receptor AVPR2, it is a nephrogenic diabetes insipidus in acquired or hereditary form. We can make difference on AVP levels and/or on desmopressine response which is negative in nephrogenic forms. Hyponatremia occurs when there is an excess of ADH production: it is a euvolemic hypoosmolar hyponatremia. The most frequent etiology is SIADH (syndrome of inappropriate secretion of ADH), a diagnostic of exclusion which is made after eliminating corticotropin deficiency and hypothyroidism. In case of brain injury the differential diagnosis of cerebral salt wasting (CSW) syndrome has to be discussed, because its treatment is perfusion of isotonic saline whereas in SIADH, the treatment consists in administration of hypertonic saline if hyponatremia is acute and/or severe. If not, fluid restriction demeclocycline or vaptans (antagonists of V2 receptors) can be used in some European countries. Four types of SIADH exist; 10 % of cases represent not SIADH but SIAD (syndrome of inappropriate antidiuresis) due to a constitutive activation of vasopressin receptor that produces water excess. c 2013 Published by Elsevier Masson SAS.
authors.affiliation: Service d'endocrinologie, Maladies métaboliques et nutrition, CHU d'Amiens, place Victor-Pauchet, 80054 Amiens, France. Electronic address: karaca.pelin@chu-amiens.fr.
authors.forename: P
authors.initials: P
authors.lastname: Karaca
authors.affiliation: Service d'endocrinologie, Maladies métaboliques et nutrition, CHU d'Amiens, place Victor-Pauchet, 80054 Amiens, France.
authors.forename: R
authors.initials: R
authors.lastname: Desailloud
mesh_terms: D003919:Diabetes Insipidus / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D018500:Diabetes Insipidus, Nephrogenic / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D003937:Diagnosis, Differential; D006801:Humans; D006955:Hypernatremia / Q000209:etiology* / Q000628:therapy; D007010:Hyponatremia / Q000209:etiology* / Q000628:therapy; D007177:Inappropriate ADH Syndrome / Q000150:complications / Q000175:diagnosis; D010900:Pituitary Diseases / Q000150:complications / Q000235:genetics / Q000503:physiopathology; D010904:Pituitary Gland, Posterior / Q000378:metabolism; D017483:Receptors, Vasopressin / Q000502:physiology; D012965:Sodium Chloride / Q000008:administration & dosage; D014667:Vasopressins / Q000502:physiology*; D014883:Water-Electrolyte Imbalance / Q000503:physiopathology
chemical_list: C585768:AVPR2 protein, human; D017483:Receptors, Vasopressin; D014667:Vasopressins; D012965:Sodium Chloride
keywords: AVP; Diabetes insipidus; Diabète insipide; Hyponatremia; Hyponatrémie; SIAD; SIADH