Diabetes Insipidus: an Update

• Autores: Julie Refardt, Bettina Winzeler, Mirjan Christ-Crain
• Localización: Endocrinology and metabolism clinics of North America, ISSN 0889-8529, Vol. 49, Nº. 3, 2020 (Ejemplar dedicado a: Pituitary Disorders), págs. 517-531
• Idioma: inglés
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• Resumen

  • Diabetes insipidus is one of the main causes of the polyuria polydipsia syndrome and is characterized by a high hypotonic urinary output of more than 50 mL/kg body weight per 24 hours, accompanied by polydipsia of more than 3 L/d.1 After exclusion of osmotic diuresis (such as uncontrolled diabetes mellitus), the differential diagnosis of diabetes insipidus involves the distinction between primary forms (with central or renal origin) and secondary forms of polyuria (resulting from primary polydipsia). Central diabetes insipidus, also called hypothalamic or neurogenic diabetes insipidus, results from inadequate secretion and usually deficient synthesis of arginine vasopressin (AVP) in the hypothalamic neurohypophyseal system in response to osmotic stimulation. It is mostly acquired owing to disorders that disrupt the neurohypophysis