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Geetha Maddukuri

, MD, Saint Louis University

Last full review/revision Jan 2021| Content last modified Jan 2021
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Polyuria is urine output of > 3 L/day; it must be distinguished from urinary frequency, which is the need to urinate many times during the day or night but in normal or less-than-normal volumes. Either problem can include nocturia.

Pathophysiology of Polyuria

Water homeostasis is controlled by a complex balance of water intake (itself a matter of complex regulation), renal perfusion, glomerular filtration and tubular reabsorption of solutes, and reabsorption of water from the renal collecting ducts.

When water intake increases, blood volume increases and blood osmolality decreases, decreasing release of antidiuretic hormone (ADH; also referred to as arginine vasopressin) from the hypothalamic-pituitary system. Because ADH promotes water reabsorption in the renal collecting ducts, decreased levels of ADH increase urine volume, allowing blood osmolality to return to normal.

Additionally, high amounts of solutes within the renal tubules cause a passive osmotic diuresis (solute diuresis) and thus an increase in urine volume. The classic example of this process is the glucose-induced osmotic diuresis in uncontrolled diabetes mellitus, when high urinary glucose levels (> 250 mg/dL [13.88 mmol/L]) exceed tubular reabsorption capacity, leading to high glucose levels in the renal tubules; water follows passively, resulting in glucosuria and increased urine volume. Glucose-induced osmotic diuresis in diabetes mellitus is further increased with use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) that lower plasma glucose levels by inhibiting renal glucose reabsorption and increasing renal glucose excretion.

Therefore, polyuria results from any process that involves

Etiology of Polyuria

The most common cause of polyuria in adults is

  • Taking diuretics

The most common cause of polyuria (see table Some Causes of Polyuria) in adults and children is

In the absence of diabetes mellitus, the most common causes are


Some Causes of Polyuria


Suggestive Findings

Diagnostic Approach*

Water diuresis

Central diabetes insipidus (partial or complete)

  • Inherited

  • Acquired (due to injury, tumors, or other lesions)

Abrupt or chronic onset of thirst and polyuria

Sometimes follows trauma, pituitary surgery, or hypoxic or ischemic cerebrovascular insult or occurs during the first few weeks of life

Laboratory tests

Water deprivation test with ADH challenge

ADH measurement when diagnosis remains unclear

Nephrogenic diabetes insipidus

Gradual onset of thirst and polyuria in a patient with:

  • A history of lithium use for bipolar disorder

  • Hypercalcemia related to hyperparathyroidism

  • Family members who drink excess amounts of water (in children)

  • An underlying paraneoplastic disorder (possibly causing hypercalcemia)

  • Age within the first few years of life

Laboratory tests

Water deprivation test with ADH challenge


  • Primary (hypothalamic lesions in the hypothalamic thirst center)

  • Psychogenic

Anxious, middle-aged woman

History of psychiatric illnesses

Infiltrating lesions of the hypothalamus (usually sarcoidosis)

Laboratory tests

Water deprivation test with ADH challenge

Excessive hypotonic IV fluid administration

Hospitalized patient receiving IV fluids

Possibly edema

Resolution after fluids stopped or rate of administration decreased

Diuretic use

Recent initiation of diuretic for volume overload (eg, due to heart failure or peripheral edema)

Patients who are likely to surreptitiously use diuretics for weight loss (eg, those with eating disorders or concerns about weight, athletes, adolescents)

Clinical evaluation

Adipsic diabetes insipidus (a hypothalamic disorder characterized by a loss of thirst in response to hypernatremia accompanied by diabetes insipidus)

Polyuria without excessive thirst

Sometimes lesions in the hypothalamic region, such as a germinoma or craniopharyngioma, or recent anterior communicating artery repair

Sometimes hyperosmolality (eg, 300 to 340 mOsm/kg [or mmol/kg]) and hypernatremia without excessive thirst

Gestational diabetes insipidus (resulting from increased ADH metabolism)

Polydipsia (with excessive thirst) and polyuria that develop for the first time during the 3rd trimester

Inappropriately normal plasma sodium (normally decreases by about 5 mEq/L [or mmol/L] in late pregnancy) with urine osmolality lower than plasma osmolality

Resolution 2–3 weeks postpartum

Solute diuresis†

Uncontrolled diabetes mellitus

Thirst and polyuria in a young child or in an obese adult with family history of type 2 diabetes

Finger-stick glucose measurement

Isotonic or hypertonic saline infusions

Hospitalized patient receiving IV fluids

Laboratory tests (eg, 24-hour urine collection showing total osmole excretion [osmolality × urine volume])

Stopping or slowing rate of administration (to confirm that polyuria resolves)

High-protein tube feedings

Any patient receiving tube feedings

Switching to tube feedings with lower protein content (to confirm that polyuria resolves)

Polyuria after bladder catheterization in a patient with bladder outlet obstruction

Clinical evaluation

* Most patients should have measurement of urine and plasma osmolarity and serum sodium.

† Urine osmolality is typically < 300 mOsm/kg (300 mmol/kg) in water diuresis and > 300 mOsm/kg (300 mmol/kg) in solute diuresis.

ADH = antidiuretic hormone.

Evaluation of Polyuria


History of present illness should include the amounts of fluid consumed and voided to distinguish between polyuria and urinary frequency. If polyuria is present, patients should be asked about the age at onset, rate of onset (eg, abrupt vs gradual), and any recent clinical factors that may cause polyuria (eg, IV fluids, tube feedings, resolution of urinary obstruction, stroke, head trauma, surgery). Patients should be asked about their degree of thirst.

Review of systems should seek symptoms suggesting possible causes, including dry eyes and dry mouth (Sjögren syndrome) and weight loss and night sweats (cancer).

Past medical history should be reviewed for conditions associated with polyuria, including diabetes mellitus, psychiatric disorders, sickle cell disease, sarcoidosis, amyloidosis, and hyperparathyroidism. A family history of polyuria and excessive water drinking should be noted. Drug history should note use of any drugs associated with nephrogenic diabetes insipidus (see table Some Causes of Polyuria) and agents that increase urine output (eg, diuretics, alcohol, caffeinated beverages).

Physical examination

The general examination should note signs of obesity (as a risk factor for type 2 diabetes mellitus) or undernutrition or cachexia that might reflect an underlying cancer or an eating disorder plus surreptitious diuretic use.

The head and neck examination should note dry eyes or dry mouth (Sjögren syndrome). Skin examination should note the presence of any hyperpigmented or hypopigmented lesions, ulcers, or subcutaneous nodules that may suggest sarcoidosis. Comprehensive neurologic examination should note any focal deficits that suggest an underlying neurologic insult and assess mental status for indications of a thought disorder. Volume status should be assessed. Extremities should be examined for edema.

Red flags

The following findings are of particular concern:

  • Abrupt onset or onset during the first few years of life

  • Night sweats, cough, and weight loss, especially when there is an extensive smoking history

  • Psychiatric disorder

Interpretation of findings

History can often distinguish polyuria from frequency, but rarely a 24-hour urine collection may be needed.

Clinical evaluation may suggest a cause (see table Some Causes of Polyuria), but testing is usually necessary. Diabetes insipidus is suggested by a history of cancer or chronic granulomatous disease (due to hypercalcemia), use of certain drugs (lithium, cidofovir, foscarnet, ifosfamide), and less common conditions (eg, sickle cell disease, renal amyloidosis, sarcoidosis, Sjögren syndrome) that have manifestations that are often more prominent than and precede the polyuria.

Abrupt onset of polyuria at a precise time suggests central diabetes insipidus, as does preference for extremely cold or iced water. Onset during the first few years of life is typically related to inherited central or nephrogenic diabetes insipidus or uncontrolled type 1 diabetes mellitus. Polyuria caused by solute diuresis is suggested by a history of diabetes mellitus. Psychogenic polydipsia is more common in patients with a history of a psychiatric disorder (primarily bipolar disorder, or schizophrenia) rather than as an initial manifestation.


Once excess urine output has been verified by history or measurements, serum or fingerstick glucose determination should be done to rule out uncontrolled diabetes.

If hyperglycemia is not present, then testing is required:

  • Serum and urine chemistries (electrolytes, calcium)

  • Serum and urine osmolality and sometimes plasma antidiuretic hormone (ADH) level

These tests look for hypercalcemia, hypokalemia (due to surreptitious diuretic use), and hypernatremia or hyponatremia:

  • Hypernatremia (sodium > 142 mEq/L [142 mmol/L]) suggests excess free water loss due to central or nephrogenic diabetes insipidus.

  • Hyponatremia (sodium < 137 mEq/L [137 mmol/L]) suggests excess free water intake secondary to polydipsia.

  • Urine osmolality is typically < 300 mOsm/kg (300 mmol/kg) with water diuresis and > 300 mOsm/kg (300 mmol/kg) with solute diuresis.

If the diagnosis remains unclear, then measurement of serum and urine sodium and osmolality in response to a water deprivation test and exogenous ADH administration should be done. Because serious dehydration may result from this testing, the test should be done only while patients are under constant supervision; hospitalization is usually required. Additionally, patients in whom psychogenic polydipsia is suspected must be observed to prevent surreptitious drinking.

Various protocols can be used in water deprivation tests. Each protocol has some limitations. Typically, the test is started in the morning by weighing the patient, obtaining venous blood to determine serum electrolyte concentrations and osmolality, and measuring urine osmolality. Voided urine is collected hourly, and its osmolality is measured. Dehydration is continued until orthostatic hypotension and postural tachycardia appear, 5% of the initial body weight has been lost, or the urinary concentration does not increase > 30 mOsm/kg (30 mmol/kg) in sequentially voided specimens. Serum electrolytes and osmolality are again determined, and 5 units of aqueous vasopressin are injected subcutaneously. Urine for osmolality measurement is collected one final time 60 minutes postinjection, and the test is terminated.

A normal response produces maximum urine osmolality after dehydration (> 700 mOsm/kg [700 mmol/kg]), and osmolality does not increase more than an additional 5% after injection of vasopressin.

In central diabetes insipidus, patients are typically unable to concentrate urine to greater than the plasma osmolality but are able to increase their urine osmolality after vasopressin administration. The increase in urine osmolality is 50 to 100% in central diabetes insipidus vs 15 to 45% with partial central diabetes insipidus.

In nephrogenic diabetes insipidus, patients are unable to concentrate urine to greater than the plasma osmolality and show no additional response to vasopressin administration. Occasionally in partial nephrogenic diabetes insipidus, the increase in urine osmolality can be up to 45%, but overall these numbers are much lower than those that occur in partial central diabetes insipidus (usually < 300 mOsm/kg [300 mmol/kg]).

In psychogenic polydipsia, urine osmolality is < 100 mOsm/kg (100 mmol/kg). Decreasing water intake gradually will lead to decreasing urine output, increasing plasma and urine osmolality and serum sodium concentration.

Measurement of circulating ADH is the most direct method of diagnosing central diabetes insipidus. Levels at the end of the water deprivation test (before the vasopressin injection) are low in central diabetes insipidus and appropriately elevated in nephrogenic diabetes insipidus. However, ADH levels are not routinely available. In addition, water deprivation is so accurate that direct measurement of ADH is rarely necessary. If measured, ADH levels should be checked at the beginning of the water deprivation test, when the patient is well hydrated; ADH levels should increase as intravascular volume decreases.

Treatment of Polyuria

Treatment varies by cause. Troubling nocturia can be managed by measures such as reducing fluid intake before bedtime, the use of desmopressin, and/or improving sleep hygiene.

Key Points

  • Use of diuretics and uncontrolled diabetes mellitus are common causes of polyuria.

  • In the absence of diabetes mellitus and diuretic use, the most common causes of chronic polyuria are primary polydipsia, central diabetes insipidus, and nephrogenic diabetes insipidus.

  • Hypernatremia can indicate central or nephrogenic diabetes insipidus.

  • Hyponatremia is more characteristic of polydipsia.

  • Abrupt onset of polyuria suggests central diabetes insipidus.

  • A water deprivation test can help with diagnosis but should only be done with the patient under close supervision.

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