Some Causes of Polyuria

Cause

Suggestive Findings

Diagnostic Approach*

Water diuresis

(AVP-D) (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

(AVP-R)

Gradual onset of thirst and polyuria in a patient with:

  • 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

Polydipsia

  • Primary (hypothalamic lesions causing defect 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 (ADI) (a hypothalamic disorder characterized by absent thirst from loss of osmoreceptor function and polyuria from AVP deficiency accompanied byhypernatremia)

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 third 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)

Relief of urinary tract obstruction

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.

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