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Nephrogenic diabetes insipidus

Diabetes insipidus (DI) is a disease characterized by excretion of large amounts of severely diluted urine, which cannot be reduced when fluid intake is reduced. It denotes inability of the kidney to concentrate urine. DI is caused by a deficiency of antidiuretic hormone, or by an insensitivity of the kidneys to that hormone. more...

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Signs and symptoms

Excessive urination and extreme thirst (especially for cold water) are typical for DI. Symptoms of diabetes insipidus are quite similar to those of severely deranged diabetes mellitus, with the distinction that the urine is not sweet and there is no hyperglycemia (elevated blood glucose). Blurred vision is a rarity.

The extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain, and growth as well. They may present with fever, vomiting, or diarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is drunk to offset the urinary losses. However, there is a continuous risk of dehydration.


In order to distinguish DI from other causes of excess urination, blood glucose, bicarbonate and calcium need to be tested. Electrolytes can show substantial derangement; hypernatremia (excess sodium levels) are common in severe cases. Urinalysis shows low electrolyte levels, and measurement of urine osmolarity (or specific gravity) is generally low.

A fluid deprivation test helps determine whether DI is caused by:

  1. excessive intake of fluid
  2. a defect in ADH production
  3. a defect in the kidneys' response to ADH

This test measures changes in body weight, urine output, and urine composition when fluids are withheld. Sometimes measuring blood levels of ADH during this test is also necessary.

To distinguish between the main forms, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet. While taking desmopressin, a patient should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in central DI. If desmopressin reduces urine output and increases osmolarity, the pituitary production of ADH is deficient, and the kidney responds normally. If the DI is due to renal pathology, desmopressin does not change either urine output or osmolarity.

If central DI is suspected, testing of other hormones of the pituitary, as well as magnetic resonance imaging (MRI), is necessary to discover if a disease process (such as a prolactinoma) is affecting pituitary function.


Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium. In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels.

The regulation of urine production is the hypothalamus, which produces antidiuretic hormone (ADH or vasopressin) in the posterior lobe of the pituitary gland. In addition, it regulates the sensation of thirst as perceived by the cortex.


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Caring for patients with diabetes insipidus
From Nursing, 5/1/96 by Davies, Patricia


Characterized by profound diuresis of dilute urine, diabetes insipidus (DI) is a metabolic disorder that occurs when the body can't secrete or utilize antidiuretic hormone (ADH). Normally, when the body needs to conserve water, the posterior pituitary releases ADH to maintain normal plasma volume and homeostasis. But two types of DI can impede the process.

* Neurogenic DI occurs when ADH-producing cells in the hypothalamus are damaged or the pituitary can't release ADH when stimulated. Causes include trauma to the neurohypophysis, an intracranial tumor, neurosurgery, or an unknown factor. If cerebral edema is a factor, the DI may resolve in days or weeks, when the edema subsides. But extensive destruction of ADH-producing hypothalamic cells or tissue in the posterior pituitary causes permanent DI.

* Nephrogenic DI is rare. It occurs when a chronic renal disease, such as polycystic kidneys or pyelonephritis, prevents the renal tubules from reabsorbing water in response to ADH.


Polyuria, polydipsia, and dehydration are the hallmarks of DI. The patient may produce from 3 to 15 liters (3.2 to 15.8 quarts) of urine daily with a specific gravity of 1.005 or less. Typically, polyuria begins abruptly and reaches its peak in 1 or 2 days. Although the patient craves cold liquids, he may be unable to drink enough to replenish his fluid loss. As a result, he may develop dry mucous membranes and doughy skin turgor; his saliva and sweat production may decrease.


If DI persists, the patient may develop hypovolemia electrolyte imbalances. Hypovolemia can lead to hypotension and decreased systemic perfusion. Without adequate fluid replacement, hypernatremia may affect the patient's cerebral function, causing decreased level of consciousness or coma.


Plasma and urine osmolality (ion concentration) are the keys to diagnosing DI. As the patient's blood loses water, plasma osmolality increases--typically to greater than 300 mOsm/kg H sub 2 O (normal, 280 to 295 mOsm/kg H sub 2 O). As the kidneys flush water from his body, urine osmolality decreases--typically to less than 200 mOsm/kg H sub 2 O (normal, 300 to 1,000 mOsm/kg H sub 2 O). Consequently, urine specific gravity drops, serum electrolyte levels rise, and the patient loses weight as he becomes dehydrated.

You can perform a fluid deprivation test (which may last 6 to 18 hours) to determine whether your patient's DI is neurogenic or nephrogenic. To perform the test, follow these steps:

* Obtain a baseline plasma osmolality level and weigh the patient. Then begin withholding his fluids.

* Every hour, measure his urine output, osmolality, and specific gravity and monitor his overall condition, such as mental status and vital signs, for signs and symptoms of dehydration.

* Weigh your patient if signs and symptoms of dehydration worsen. If he loses 2 kg (4.4 pounds) or more or develops hypotension, tachycardia, or lethargy, discontinue the test and notify his physician.

* When two consecutive urine osmolality levels vary by less than 30 mOsm/kg H sub 2 O, measure your patient's plasma osmolality level. Then administer five units of aqueous vasopressin (exogenous ADH). One hour later, again measure his urine osmolality and compare the results with the baseline value.

If your patient has neurogenic DI, his urine osmolality will increase after vasopressin administration; if he has nephrogenic DI, he won't respond to vasopressin.


Interventions for a patient with DI are related to fluid deficit caused by DI or treatment-induced water retention.

* Manage your patient's fluid replacement by providing oral liquids or administering intravenous fluids, as prescribed. Assess his intake and output every hour, and look for signs of dehydration. Measure urine specific gravity every 2 hours.

* Assess his vital signs every 2 hours. Tachycardia, hypotension, and orthostatic hypotension signal hypovolemia; hypertension may indicate water intoxication.

* Monitor for hypernatremia and hyperosmolality by assessing serum electrolyte levels and plasma osmolality, as prescribed.

* Monitor for changes in behavior, mood, anxiety level, and level of consciousness, which may indicate altered cerebral function. Provide uninterrupted rest periods.

* Administer exogenous ADH, as prescribed, and monitor for decreased urine output, hyponatremia, increased blood pressure, tremors, or headache. If these signs and symptoms of systemic water retention develop, notify the physician--she may need to reduce your patient's dosage.

* Weigh your patient daily. A weight gain or loss of 1.4 kg (3 pounds) or more over 2 to 3 days indicates fluid accumulation or loss.

* Teach your patient about DI, his medication, and the need for follow-up care. Review the signs and symptoms of water intoxication, which may signal the return of ADH function or the need for a reduction in his medication dosage.

Copyright Springhouse Corporation May 1996
Provided by ProQuest Information and Learning Company. All rights Reserved

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