Open AccessWater, lithium and sodium: watch out for dangerous injuries
Author(s) -
Martin Fayolle,
Jean-Sébastien Souweine,
Olivier Mathieu,
Anne-Sophie Bargnoux,
JeanPaul Cristol,
Stéphanie Badiou
Publication year - 2020
Publication title -
annales de biologie clinique
Language(s) - English
Resource type - Journals
eISSN - 1950-6112
pISSN - 0003-3898
DOI - 10.1684/abc.2020.1570
Subject(s) - nephrogenic diabetes insipidus , polyuria , hypernatremia , diabetes insipidus , polydipsia , medicine , aquaporin 2 , lithium (medication) , desmopressin , endocrinology , hyponatremia , thirst , diabetes mellitus , chemistry , sodium , water channel , mechanical engineering , engineering , inlet , organic chemistry
Nephrogenic diabetes insipidus due to the inability of the kidneys to concentrate urine is frequently observed during lithium therapy. Lithium concentrates into principal cells in collecting ducts in the kidney and downregulates aquaporin 2 expression, which reduces renal reabsorption of water. This disease is characterized by polyuria - polydipsia leading to intracellular dehydration and hypernatremia. Water deprivation test is performed to confirm insipidus diabetes. The desmopressin permits to distinguish nephrogenic from cranial insipidus diabetes. We report the case of a 64 years old women who presented with global dehydration and severe hypernatremia. Four years ago, she was hospitalized for nephrogenic diabetes insipidus related to a self-induced lithium intoxication. Persistent nephrogenic insipidus diabetes after cessation of lithium therapy are described in literature, and this hypothesis may be consistent with this case report.