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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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Recognizing lithium-induced diabetes insipidus
From Nursing, 6/1/02 by Innis, Jennifer


With long-term use, this drug can damage the kidneys. Here's how to respond.

Fred Zane is in your unit after being brought to the emergency department (ED) by ambulance. He was found wandering on the street, dazed and incontinent of urine.

He answers all questions by saying, "I don't know" Two bottles of medication were found in his coat pocket: one for lithium and one for lorazepam.

The report from the ED nurse notes that Mr. Zane, 52, is alert and oriented to person only. During the past 8 hours, he's produced 3 liters of dilute yellow urine. A computed tomography scan of the head showed no mass infarct, bleeding, or trauma. His serum sodium level is 150 mEq/liter (normal, 133 to 147 mEq/liter).

Whenever a patient has polyuria (excessive urine output) or polydipsia (excessive thirst), you need to rule out endocrine problems such as diabetes mellitus or diabetes insipidus (DI). Mr. Zane is presumptively diagnosed with DI.

Because of his extreme fluid loss, Mr. Zane develops dry mucous membranes and poor skin turgor, which are signs of dehydration. Without treatment, he'll develop hypovolemic shock, manifested in its late stages as tachycardia and hypotension, and finally shock and death.

How trouble occurred

As Mr. Zane became dehydrated from his excessive urine output, his serum osmolality rose. You note his serum osmolality at 310 mOsm/kg (normal, 280 to 300 mOsm/kg) in his admission lab studies from the ED. Remember, an increase in osmolality means an increase in the amount of solute in the blood.

When plasma osmolality is above 290 mOsm/kg, osmoreceptors in the hypothalamus are stimulated and antidiuretic hormone (ADH) is released from the posterior pituitary. The osmoreceptors also trigger central thirst mechanisms so that the patient with increased osmolality is thirsty.

Antidiuretic hormone causes greater permeability to water in the renal distal tubules. In other words, ADH makes the tubules hold on to water instead of excreting it as urine.

When serum osmolality is less than 285 mOsm/kg, a normal value for the ADH level is less than 2.2 picograms/ml. When serum osmolality is greater than 285 mOsm/kg, a normal ADH value is 2.2 to 8.5 picograms/ml.

With serum osmolality of 310 mOsm/kg, Mr. Zane's ADH level is 10.7. His hypothalamus is secreting ADH in response to his high serum osmolality. However, lithium has damaged the kidneys' distal tubules, which are having difficulty responding to the ADH.

Treating Mr. Zane

Your treatment focuses on rehydration. You give intravenous fluid replacement and push PO. fluids, first ensuring that Mr. Zane is awake and alert to protect his airway and prevent aspiration. As with all patients with DI, you closely monitor his intake and output.

Patients with nephrogenic DI may start treatment with thiazide diuretics, which help the kidneys excrete sodium and decrease the glomerular filtration rate. This helps to decrease the amount of water that reaches the distal tubules.

The physician starts Mr. Zane on hydrochlorothiazide, 25 mg PO. twice daily. Because thiazide diuretics are usually used in treating hypertension, monitor Mr. Zane's blood pressure carefully.

Besides thiazide diuretics, nonsteroidal anti-- inflammatory drugs (NSAIDs) are thought to help patients with nephrogenic DI. NSAIDs decrease the release of renal prostaglandins, which are present when the kidneys are damaged. If NSAIDs can decrease the effects of the prostaglandins, less water will be delivered to the distal tubules, which could help decrease urine output. Mr. Zane is also started on 50 mg of oral indomethacin every 8 hours.

Lithium, which is almost entirely eliminated by the kidneys, is one cause of nephrogenic DI. You recall that lithium was one medication found in Mr. Zane's pocket on his admission to the ED. A patient doesn't need to experience lithium toxicity to develop DI; Mr. Zane had a normal lithium level of 0.9 mmol/liter (normal range, 0.6 to 1.2 mmol/liter).

After this episode, Mr. Zane is transferred to the psychiatric unit. His lithium is discontinued and he's switched to gabapentin (Neurontin), an anti-- convulsant drug not indicated for treating bipolar illness but sometimes used to treat patients with this condition.


Goroll, A., et al.: Primary Care Medicine: Office Evaluation and Management of the Adult Patient, 4th edition. Philadelphia, Pa., Lippincott Williams & Wilkins, 2000.

Heater, D.: "If ADH Goes Out of Balance: Diabetes Insipidus," RN. 62(7):44-46,july 1999.

Mukhopadhyay, D., et al.: "Lithium-induced Nephrogenic Diabetes Insipidus in Older People," Age & Ageing. 30(4):347-350, July 2001. Nickolaus, M.: "Diabetes Insipidus: A Current Perspective," Critical Care Nurse. 19(6):18-30, December 1999.

Waise, A., and Fisken, R.: "Unsuspected Nephrogenic Diabetes Insipidus," British Medical Journal. 323(7304):96-97, July 14, 2001.


Jennifer Innis is an acute care nurse practitioner at St Michael's Hospital in Toronto, Ontario.

Copyright Springhouse Corporation Jun 2002
Provided by ProQuest Information and Learning Company. All rights Reserved

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