Overview of diabetes insipidus

Diabetes insipidus is defined by a reduced reabsorption of water from the kidneys back into the circulation, leading to polyuria, polydipsia and electrolyte imbalances (particularly hypernatraemia). If untreated, it can cause severe dehydration and seizures. Diabetes insipidus can be caused by arginine vasopressin (AVP) (also known as antidiuretic hormone) deficiency due to hypopituitarism (central diabetes insipidus), or by reduced sensitivity to arginine vasopressin in the kidneys (nephrogenic diabetes insipidus).

Central diabetes insipidus most commonly occurs as a transient complication of pituitary surgery, although it can be ongoing. Patients with uncomplicated pituitary adenomas rarely develop diabetes insipidus—its presence without a history of pituitary surgery (or other acute cause such as head injury or stroke) suggests a sellar or parasellar mass other than an adenoma (eg craniopharyngioma, metastatic malignancy, germinoma, inflammatory disorder such as lymphocytic hypophysitis or Langerhans cell histiocytosis).

Refer patients with new-onset diabetes insipidus without an obvious precipitant to an endocrinologist for a water deprivation test to confirm the diagnosis. A water deprivation test involves measurement of the response of plasma and urine osmolality to desmopressin during closely supervised water deprivation. The urine osmolality will increase in response to desmopressin if the patient has central diabetes insipidus, but not nephrogenic diabetes insipidus.

New-onset diabetes insipidus with an obvious acute precipitant (eg head injury, pituitary surgery) does not require a water deprivation test to confirm the diagnosis.