ABSTRACT:
Antidiuretic hormone (ADH), also known as arginine vasopressin (AVP), plays a central role in conserving body water. It is synthesised by magnocellular neurons in the hypothalamic supraoptic and paraventricular nuclei and released from the posterior pituitary when plasma osmolality increases or effective circulating volume falls. In the kidney, AVP binds to V2 receptors and promotes the insertion of aquaporin-2 water channels into the apical membrane of collecting-duct cells. When AVP synthesis or secretion is impaired, the resulting condition is central diabetes insipidus (CDI), increasingly referred to as arginine vasopressin deficiency (AVP-D). It is characterised by hypotonic polyuria and compensatory polydipsia, with a risk of dehydration and hypernatraemia when water intake cannot keep pace with losses. This review examines the physiology and causes of AVP-D, current diagnostic approaches—including stimulated copeptin testing—and contemporary management. Particular attention is given to post-operative disease, special clinical populations, treatment-related hyponatraemia, and gaps in the evidence that need to be addressed.