Polyuria: A Merck Manual of Patient Symptoms podcast
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.
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 ADH (also referred to as argininevasopressin) 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) exceed tubular reabsorption capacity, leading to high glucose levels in the renal tubules; water follows passively, resulting in glucosuria and increased urine volume.
Therefore, polyuria results from any process that involves
The most common cause of polyuria in adults is
The most common cause of polyuria (see Table 3: Some Causes of Polyuria) in both adults and children is
In the absence of diabetes mellitus, the most common causes are
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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 3: Some Causes of Polyuria) and agents that increase urine output (eg, diuretics, alcohol, caffeinated beverages).
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.
The following findings are of particular concern:
Interpretation of findings:
History can often distinguish polyuria from frequency, but rarely a 24-h urine collection may be needed.
Clinical evaluation may suggest a cause (see Table 3: 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:
These tests look for hypercalcemia, hypokalemia (due to surreptitious diuretic use), and hypernatremia or hyponatremia:
If the diagnosis remains unclear, then measurement of serum and urine Na 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 in sequentially voided specimens. Serum electrolytes and osmolality are again determined, and 5 units of aqueous vasopressin are injected sc. Urine for osmolality measurement is collected one final time 60 min postinjection, and the test is terminated.
A normal response produces maximum urine osmolality after dehydration (> 700 mOsm/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 (see Central Diabetes Insipidus). 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 (see Nephrogenic Diabetes Insipidus). 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).
In psychogenic polydipsia, urine osmolality is < 100 mOsm/kg. Decreasing water intake gradually will lead to decreasing urine output, increasing plasma and urine osmolality and serum Na 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 varies by cause.
Last full review/revision July 2013 by Anuja P. Shah, MD
Content last modified November 2013