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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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Transient acquired diabetes insipidus after vasopressin therapy for hypotension: a case report
From CHEST, 10/1/05 by Christian Ramers

INTRODUCTION: Vasopressin use has increased after being shown to be an effective adjunct for adrenergic-refractory septic shock. Adverse events from vasopressin infusions included decreased cardiac output and vasoconstriction causing hypoperfusion to the skin, gut and coronary arteries. We report a case of acute hypernatremia after discontinuation of vasopressin for the treatment of septic shock.

CASE PRESENTATION: A 34 year old male presented to our intensive care unit with hypercarbic respiratory failure due to obesity-hypoventilation syndrome and pneumonia. On hospital day #3, he developed hypotension requiring norepinephrine and eventually, vasopressin. Empiric antifungal therapy was started given extensive epidermal yeast infection. Blood cultures eventually grew Candida glabrata. On hospital day #6, norepinephrine and vasopressin were discontinued. A brisk diuresis followed: the patient urinated 12 Liters in 8 hours, serum sodium climbed from 146 to 171 mmol/L and urine osmolarity fell to 116 mOsm/kg (normal 250-1200) (Figure 1). This profound hypoosmotic diuresis ceased with exogenous DDAVP, consistent with an acquired diabetes insipidus. To maintain eunatremia, he required scheduled and then intermittent doses of DDAVP until hospital day #47. Head computed tomography revealed no pituitary or hypothalamic lesions.


DISCUSSIONS: Vasopressin is a peptide hormone secreted by the posterior pituitary involved in both the regulation of serum osmolality and maintenance of adequate perfusion pressure. High serum osmolality and hypotension stimulate vasopressin release, but hypotension is a more potent stimulus. Vasopressin acts on the endothelium causing vasoconstriction and in the distal convoluted tubule and collecting ducts to facilitate reabsorption of free water. Vasopressin has been used to treat nocturnal eneuresis, GI hemorrhage, diabetes insipidus, some forms of yon Willebrand's disease, hemophilia A, and as an alternative to epinephrine in cardiac arrest. Recently vasopressin has been used at physiologic doses for vasodilatory shock: post CABG or in sepsis. Investigators rationalize that low doses of vasopressin replete vasopressin stores in the pro-inflammatory state, improving sensitivity to cathecholamines. In small, randomized controlled trials, vasopressin infusion allowed greater dose reductions of other vasopressors when compared to placebo. Reported side effects of vasopressin include: arterial and venous thromboembolism, pseudotumor cerebri, torsades des pointes, myocardial infarction, rhabdomyolysis, skin necrosis, and disorders of sodium homeostasis. Most of these adverse events were observed with the higher doses of vasopressin used for GI hemorrhage, but some have been reported with the doses used in sepsis. One prior report described hypernatremia following discontinuation of vasopressin therapy, but the patient had a history of SIADH. We believe our patient's central diabetes insipidus was iatrogenic-related to the discontinuation of a continuous vasopressin infusion. The mechanism is speculative, but may be due to antibody-mediated competitive inhibition of the hormone which may be overcome by additional exogenous replacement.

CONCLUSION: The phenomenon of acquired transient diabetes insipidus may represent a rare adverse reaction to vasopressin therapy in patients with septic shock.


(1) Holmes CL, Patel BM, Russell JA, et al. Physiology of vasopressin relevant to management of septic shock. Chest 2001; 120:989-1002

(2) Sharshar T, Carlier R, Blanchard A, et al. Depletion of neurohypophyseal content of vasopressin in septic shock. Crit Care Med 2002; 30:497-500

(3) Patel BM, Chittock DR, Russell JA, et al. Beneficial effects of short-term vasopressin infusion during severe septic shock. Anesthesiology 2002; 96:576-582

(4) Holmes CL, Walley KR, Chittock DR, et al. The effects of vasopressin on hemodynamics and renal function in severe septic shock: a case series. Intensive Care Med 2001; 27:1416-1421

(5) Kristeller JL, Sterns RH. Transient diabetes insipidus after discontinuation of therapeutic vasopressin. Pharmacotherapy 2004; 24: 541-545

DISCLOSURE: Christian Ramers, None.

Christian Ramers MD * Joseph A. Govert MD Alison S. Clay MD Duke University, Durham, NC

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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