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Clinical manifestations and causes of central diabetes insipidus

Daniel G Bichet, MD
Section Editor
Richard H Sterns, MD
Deputy Editor
John P Forman, MD, MSc


Central diabetes insipidus (CDI) is characterized by decreased release of antidiuretic hormone (ADH, also called arginine vasopressin or AVP), resulting in a variable degree of polyuria. Lack of ADH can be caused by disorders that act at one or more of the sites involved in ADH secretion: the hypothalamic osmoreceptors; the supraoptic or paraventricular nuclei; or the superior portion of the supraopticohypophyseal tract [1]. By contrast, damage to the tract below the median eminence or to the posterior pituitary generally causes only transient polyuria, because ADH produced in the hypothalamus can still be secreted into the systemic circulation via the portal capillaries in the median eminence [1]. (See "Hypothalamic-pituitary axis".)

The clinical manifestations and causes of CDI will be reviewed here. The treatment of CDI, the clinical manifestations and causes of nephrogenic diabetes insipidus (DI), and the diagnostic approach to the polyuric patient are discussed separately. (See "Treatment of central diabetes insipidus" and "Clinical manifestations and causes of nephrogenic diabetes insipidus" and "Diagnosis of polyuria and diabetes insipidus".)


Patients with untreated central diabetes insipidus (CDI) typically present with polyuria, nocturia, and, due to the initial elevation in serum sodium and osmolality, polydipsia. They may also have neurologic symptoms related to the underlying neurologic disease.

The serum sodium concentration in untreated CDI is often in the high normal range, which is required to provide the ongoing stimulation of thirst to replace the urinary water losses. Moderate to severe hypernatremia can develop when thirst is impaired or cannot be expressed. This can occur in patients with central nervous system lesions who also have hypodipsia or adipsia, in adipsic young patients who have autoantibodies to the subfornical organ [2], in infants and young children who cannot independently access free water, and in the postoperative period in patients with unrecognized diabetes insipidus (DI). (See "Etiology and evaluation of hypernatremia in adults", section on 'Adipsic diabetes insipidus'.)

Patients with CDI may develop decreased bone mineral density at the lumbar spine and femoral neck, even in those treated with desmopressin (dDAVP) [3]. It is unclear how the deficiency of ADH results in bone loss, particularly since treatment fails to prevent bone disease. However, since ADH acts upon both V1 and V2 receptors and desmopressin principally upon V2 receptors, one possible mechanism is that activation of V1 receptors stimulates bone formation.

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Literature review current through: Nov 2017. | This topic last updated: Oct 19, 2017.
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