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Diagnosis of polyuria and diabetes insipidus

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


Polyuria has generally been defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children. It must be differentiated from the more common complaints of frequency or nocturia, which are not associated with an increase in the total urine output.

The following is an overview of the diagnosis of polyuria and diabetes insipidus (DI). The causes and treatment of polyuria due to central or nephrogenic DI are presented separately. (See "Clinical manifestations and causes of central diabetes insipidus" and "Clinical manifestations and causes of nephrogenic diabetes insipidus" and "Treatment of central diabetes insipidus" and "Treatment of nephrogenic diabetes insipidus".)


In the absence of a glucose-induced osmotic diuresis in uncontrolled diabetes mellitus, there are three major causes of polyuria in the outpatient setting, each of which is due to a defect in water balance leading to the excretion of large volumes of dilute urine (urine osmolality usually below 250 mosmol/kg): primary polydipsia, which is primarily seen in adults and adolescents; central DI; and nephrogenic DI [1].

Primary polydipsia — Primary polydipsia (sometimes called psychogenic polydipsia) is characterized by a primary increase in water intake. This disorder is most often seen in middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine, which can lead to the sensation of a dry mouth. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosis [1]. (See "Causes of hyponatremia in adults".)

Central DI — Central DI (also called neurohypophyseal or neurogenic DI) is associated with deficient secretion of antidiuretic hormone (ADH). This condition is most often idiopathic (possibly due to autoimmune injury to the ADH-producing cells) or can be induced by trauma, pituitary surgery, or hypoxic or ischemic encephalopathy. Rare familial cases have been described [2]. (See "Clinical manifestations and causes of central diabetes insipidus".)

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Literature review current through: Nov 2017. | This topic last updated: Sep 28, 2017.
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