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.