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Urine output in diabetes insipidus

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


Diabetes insipidus (DI) is a disorder in which polyuria due to decreased collecting tubule water reabsorption is induced by either decreased secretion of antidiuretic hormone (ADH) (central DI) or resistance to its renal effects (nephrogenic DI). In most patients, the degree of polyuria is primarily determined by the degree of ADH deficiency or resistance [1]. Thus, the urine output may range from 2 L/day with mild partial DI to over 10 to 15 L/day in patients with severe disease.

Determinants of the urine output in patients with DI will be discussed here. The diagnosis of DI and the causes and treatment of central and nephrogenic DI are presented elsewhere. (See "Diagnosis of polyuria and diabetes insipidus" and "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".)


The determinants of the urine output differ in normal subjects and those with diabetes insipidus (DI). The urine output in normals primarily reflects water intake, which leads to alterations in the plasma osmolality that are sensed by the osmoreceptors in the hypothalamus that regulate both antidiuretic hormone (ADH) release and thirst [2,3]. In addition to central osmoreceptors, peripheral osmoreceptor neurons that innervate hepatic blood vessels detect osmotic shifts in portal blood and modulate ADH release [4]. (See "General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)", section on 'Regulation of plasma tonicity'.)

Normally, an increase in water intake sequentially lowers the plasma osmolality, decreases ADH secretion, and reduces collecting tubule permeability to water; as a result, the excess water is rapidly excreted in a dilute urine. However, changes in water intake do not result in appropriate changes in urine output in patients with DI because ADH release or effect is relatively fixed. Instead, urine output is relatively constant, regardless of water intake, unless dietary salt and/or protein intake change. Suppose, for example, that a patient has moderately severe nephrogenic DI which, because of the ADH resistance, will not respond to hormone replacement. The urine osmolality in this patient cannot be raised above 150 mosmol/kg (normal maximum urine osmolality is 900 to 1200 mosmol/kg). In this setting, the excretion of solutes (primarily sodium and potassium salts and urea) is the major determinant of the urine output. If solute excretion is in the usual range (eg, 750 mosmol/kg), then the daily urine output will be 5 L/day (750 ÷ 150 = 5). In this patient, urine output will rise if solute excretion is increased and fall if solute excretion is reduced.

Thus, one way to diminish polyuria in patients with DI is to restrict salt and protein intake, which in turn will reduce the solute load and solute excretion. If, for example, solute excretion fell to 525 mosmol/day, the urine output would fall to 3.5 L/day. On the other hand, the degree of polyuria can be enhanced by increasing solute excretion, as often occurs with high-protein hyperalimentation in hospitalized patients. Each gram of protein catabolized produces about 170 mg of urea. Thus, a protein load of 70 g (1 g/kg of body weight in a 70 kg adult) will generate approximately 11.2 g of urea nitrogen, which corresponds to approximately 400 mmol of urea. At a typical urine osmolality of 300 to 500 mosmol/kg in solute diureses, an increased urea excretion of this magnitude will require a urine output of 0.8 to 1.3 liters.

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Literature review current through: Nov 2017. | This topic last updated: Apr 15, 2016.
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