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Diabetes Insipidus

  • Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD  more...
 
Updated: Jul 06, 2016
 

Practice Essentials

Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms:

  • Central (neurogenic, pituitary, or neurohypophyseal) DI, characterized by decreased secretion of antidiuretic hormone (ADH; also referred to as arginine vasopressin [AVP])
  • Nephrogenic DI, characterized by decreased ability to concentrate urine because of resistance to ADH action in the kidney [1]

Two other forms are gestational DI and primary polydipsia (dipsogenic DI); both are caused by deficiencies in AVP, but the deficiencies do not result from a defect in the neurohypophysis or kidneys.

Signs and symptoms

The predominant manifestations of DI are as follows:

  • Polyuria: The daily urine volume is relatively constant for each patient but is highly variable between patients (3-20 L)
  • Polydipsia
  • Nocturia

The most common form is central DI after trauma or surgery to the region of the pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns:

  • Transient
  • Permanent
  • Triphasic (observed more often clinically)

In infants with DI, the most apparent signs may be the following:

  • Crying
  • Irritability
  • Growth retardation
  • Hyperthermia
  • Weight loss

In children, the following manifestations typically predominate:

  • Enuresis
  • Anorexia
  • Linear growth defects
  • Fatigability

If the condition that caused DI also damaged the anterior pituitary or hypothalamic centers that produce releasing factors, patients may present with the following:

  • Excessive fatigue
  • Diminished libido or erectile dysfunction
  • Headache
  • Dry skin
  • Hair loss

Physical findings vary with the severity and chronicity of DI; they may be entirely normal or may include the following:

  • Hydronephrosis, with pelvic fullness, flank pain or tenderness, or pain radiating to the testicle or genital area
  • Bladder enlargement in some patients
  • Dehydration if the thirst mechanism is impaired or access to fluid is restricted

See Clinical Presentation for more detail.

Diagnosis

If the clinical presentation suggests DI, laboratory tests must be performed to confirm the diagnosis, as follows:

  • A 24-hour urine collection for determination of urine volume
  • Serum electrolyte concentrations and glucose level
  • Urinary specific gravity
  • Simultaneous plasma and urinary osmolality
  • Plasma ADH level

Additional studies that may be indicated include the following:

  • Water deprivation (Miller-Moses) test to ensure adequate dehydration and maximal stimulation of ADH for diagnosis
  • Pituitary studies, including magnetic resonance imaging (MRI) and measurement of circulating pituitary hormones other than ADH

See Workup for more detail.

Management

Most patients with DI can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, provide fluid replacement as follows:

  • Give dextrose and water or an intravenous fluid that is hypo-osmolar with respect to the patient’s serum; do not administer sterile water without dextrose IV
  • Administer fluids at a rate no greater than 500-750 mL/hr; aim at reducing serum sodium by approximately 0.5 mmol/L (0.5 mEq/L) every hour

Pharmacologic therapeutic options include the following:

  • Desmopressin (drug of choice for central DI [2, 3] )
  • Synthetic vasopressin
  • Chlorpropamide
  • Carbamazepine (rarely used; employed only when all other measures prove unsatisfactory)
  • Clofibrate (no longer on the US market)
  • Thiazides
  • Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin (may be used in nephrogenic DI, but only when no better options exist)

See Treatment and Medication for more detail.

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Background

Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 h) of dilute urine (< 300m Osm/kg). DI has 2 major forms: central and nephrogenic.

Central DI is characterized by decreased secretion of antidiuretic hormone (ADH)—also known as arginine vasopressin (AVP)—which gives rise to polyuria and polydipsia by diminishing the person’s ability to concentrate urine. Other terms for central DI are neurogenic, pituitary, and neurohypophyseal DI. (See Etiology, Presentation, and Workup.)

Nephrogenic DI is characterized by a decrease in the ability to concentrate urine because of resistance to ADH action in the kidney.[1] Nephrogenic DI can be observed in chronic renal insufficiency, lithium toxicity, hypercalcemia, hypokalemia, glucosuria, and tubulointerstitial disease. (See Etiology, Presentation, and Workup.)

Two other forms of DI are gestational DI and primary polydipsia. Both are caused by deficiencies in AVP, but the deficiencies do not result from a defect in the neurohypophysis or kidneys. Gestational DI results from degradation of vasopressin by a placental vasopressinase. Primary polydipsia (dipsogenic DI) results from a primary defect in osmoregulation of thirst. The exact location of the lesion is not known, but structural lesions may exist, as dipsogenic DI has been reported in tuberculous meningitis, multiple sclerosis, and neurosarcoidosis.

Rarely, DI may be hereditary.[2] Hereditary nephrogenic DI manifests in early infancy, often before the age of 1 week. Hereditary central DI typically manifests in childhood. For more information on DI in children, see Pediatric Diabetes Insipidus.

Pharmacologic treatment of DI generally involves the use of desmopressin (1-deamino-8-D-arginine vasopressin [DDAVP]), nonhormonal drugs, or both. Patients must be instructed in simple principles of water balance to avoid dehydration and water intoxication (if they are not carefully monitoring water intake). (See Treatment.)

Physiology of water balance

The normal range of plasma osmolality is between 275 and 295 mOsm/kg. The ability of the kidneys to modify the concentration of urinary solutes ranges between 50–1200 mOsm/kg. Healthy adults on a normal diet excrete 800–1200 mOsm of solute daily. Thus, to excrete 1000 mOsm of solute, the obligate urinary water excretion would be 1000 mOsm per 1200 mOsm/kg water, which translates into 0.8 kg (0.8 L) of water per day. This urine is maximally concentrated and appears dark yellow or orange in color. If this requirement for obligate water excretion is not met, solutes accumulate, leading to uremia.

Conversely the maximum volume of urine (secondary to limits imposed by renal dilutional capacity) is 20 L of water per day (1000 mOsm per 50 mOsm/kg water). This maximally dilute urine is colorless.

The maintenance of water balance in healthy humans is principally accomplished through 3 robust, interrelated determinants: thirst, AVP, and the kidneys. In addition, recognition of a fourth factor, apelin, has emerged in recent years. Apelin is a bioactive peptide that is widely distributed throughout the body. In the brain, it is expressed in supraoptic and paraventricular nuclei, as well as in other sites, and has specific receptors located on vasopressinergic neurons. Apelin acts as a potent diuretic neuropeptide that inhibits ADH release.

AVP is the primary determinant of free water excretion in the body. Its main target is the kidney, where it acts by altering the water permeability of the cortical and medullary collecting tubules. Water is reabsorbed by osmotic equilibration with the hypertonic interstitium and returned to the systemic circulation. The actions of AVP are mediated through at least 2 receptors, as follows[4, 5] :

  • V1 - Mediates vasoconstriction, enhancement of corticotrophin release, and renal prostaglandin synthesis
  • V2 - Mediates the antidiuretic response

Effects of reduced AVP or ADH

The vasoconstrictor effect of AVP is negligible in humans. No clinically significant defects in blood pressure regulation or cortisol secretion are apparent in patients with DI.

Diminished or absent ADH production can be the result of a defect in 1 or more sites in the neurohypophysis. These include the hypothalamic osmoreceptors, the supraoptic or paraventricular nuclei, and the supraopticohypophyseal tract.

Response to volume decrease

Ordinarily, a decrease in the extracellular fluid (ECF) volume elicits the following simultaneous responses:

  • Aldosterone secretion - To preserve sodium retention
  • Thirst - To raise water intake
  • AVP secretion - To increase water retention

Volume depletion activates baroreceptor mechanisms that exert similar effects on aldosterone, thirst, and AVP, whereas osmoreceptor-mediated mechanisms impact thirst and AVP secretion only.

Osmoreceptors for thirst are solute specific, responding preferentially to increased sodium levels in the ECF. Thus, elevated glucose levels in diabetes mellitus do not induce thirst; rather, the increased thirst in uncontrolled diabetes mellitus is secondary to volume depletion from osmotic diuresis.

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Etiology

DI is usually an acquired disorder, with central DI having different causes than does nephrogenic DI. In rare cases, central or nephrogenic DI may be an inherited disorder.

Central diabetes insipidus

Central DI has many possible causes. According to the literature, the principal causes of central DI and their oft-cited approximate frequencies are as follows:

  • Idiopathic - 30%
  • Malignant or benign tumors of the brain or pituitary - 25%
  • Cranial surgery - 20%
  • Head trauma - 16% [6]

Idiopathic DI

Idiopathic central DI presumably develops when cells in the hypothalamus are damaged or destroyed. Identification of antibodies against AVP-secreting cells and advances in imaging techniques have made idiopathic cases less common than they previously were.

Increasingly, the role of inflammation and autoimmunity in DI is being recognized. Cases of lymphocytic hypophysitis were possibly classified as idiopathic prior to improved imaging studies. This disorder is characterized by lymphocytic infiltration of the stalk and posterior pituitary. Magnetic resonance imaging (MRI) may show abnormalities in these structures.

Antibodies directed against vasopressin cells have been found in patients with idiopathic central DI; however, these antibodies have also been found in patients with Langerhans cell histiocytosis (LCH) or germinomas, which indicates that this finding can not be considered a reliable marker of autoimmune etiology in central DI. Indeed, reliance on AVP antibodies may delay the diagnosis of LCH or germinoma.

Given the possible diagnostic confusion, close clinical and MRI follow-up is necessary. Serial contrast-enhanced brain MRIs (every 3-6 months for the first 2 years) in patients with central DI who have pituitary stalk thickening may shorten the time to diagnosis of germinoma by as much as 1 year.

The role of human chorionic gonadotropin (hCG) in the early diagnosis of germinoma is not fully established. A negative result for hCG in the cerebrospinal fluid (CSF) does not exclude germinoma.

Tumor-associated DI

Primary intracranial tumors causing DI include craniopharyngiomas, germinomas, and pineal tumors, among others. The appearance of other hypothalamic manifestations may be delayed for as long as 10 years in these cases.

Craniopharyngioma is a benign tumor that arises from squamous cell nests in the primitive Rathke pouch. It is the most frequent pediatric intracranial neoplasm, accounting for nearly 54% of cases. Central DI insipidus and multiple pituitary hormone deficiencies are common manifestations in childhood craniopharyngiomas. Surgery is the preferred treatment.

Postoperative DI

The frequency with which DI develops after neurosurgery varies with the surgery’s scope. Approximately 10-20% of patients experience DI after transsphenoidal removal of an adenoma, compared with 60-80% of those who have undergone excision of large tumors.

Not all cases of postoperative DI are permanent. In a German study of metabolic disturbances after transsphenoidal pituitary adenoma surgery, only 8.7% of DI cases persisted for more than 3 months.[7]

Postoperative polyuria does not necessarily indicate DI. The most common causes of postoperative polyuria are excretion of excess fluid administered during surgery and an osmotic diuresis resulting from treatment for cerebral edema.[8]

DI in head trauma

Central DI can be an acute or chronic complication of head injury or subarachnoid hemorrhage.[6, 9] Risk factors for acute DI include penetrating trauma and severe head trauma.[6] Other forms of pituitary dysfunction (eg, adrenocorticotropic hormone deficiency) may accompany posttraumatic DI.[9] The dysfunction may be transient or, less commonly, may develop gradually.[10]

Hereditary central DI

Approximately 10% of central DI cases are familial (although some experts suggest that familial DI may be underdiagnosed).[11] Most of these cases show autosomal dominant inheritance and result from a defect in the AVP-NP2 gene on chromosome 20p13. The defect results in the production of mutant prohormone that is toxic to the neuron and eventually destroys it.[12, 13, 14]

There are also autosomal recessive forms of DI, which result from defects in the AVP-NP2 (AVP neurophysin) gene, as well as in the WFS1 gene. The latter gene encodes for wolframin, a tetrameric protein that may serve as a novel endoplasmic reticular calcium channel in pancreatic beta cells and neurons. Mutations in WFS1 lead to Wolfram syndrome, which is also known by the acronym DIDMOAD (Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy, Deafness).[15]

Another recessive form of central DI results from the production of biologically inactive AVP. In addition, an X-linked form of neurohypophyseal DI exists. A specific genetic defect has not been identified.[2]

Genetic testing to determine the specific etiology can obviate the search for another cause.[2] Finding a genetic anomaly will also answer recurrence risk questions for the family, and may prove to be helpful with treatment options.

Additional causes

Other causes of central DI include the following:

A study by Lee et al found that 12% of cardiac arrest survivors treated with targeted temperature management (TTM) developed central DI, with these patients demonstrating poor neurologic outcomes and high mortality rates. The study involved 385 patients, 45 of whom were confirmed to have central DI. Multivariate analysis indicated that in cardiac arrest survivors treated with TTM, independent risk factors for central DI include younger age, nonshockable rhythm, long downtime, and asphyxial cardiac arrest.[16]

Nephrogenic diabetes insipidus

In adults, nephrogenic DI most often develops as a result of lithium toxicity or hypercalcemia. Impairment of urinary concentration occurs in up to 20% of patients taking lithium, as a result of dysregulation of the aquaporin system in principal cells of the collecting duct.[17, 18] Prolonged elevation of serum calcium concentrations above 11 mg/dL (2.75 mmol/dL can also impair urinary concentrating ability.

Other causes of acquired nephrogenic DI include the following:

  • Hypokalemia
  • Renal disease - Eg, from sickle cell disease, amyloidosis
  • Pregnancy (transient)
  • Hyperglycemia (osmotic diuresis)

In addition to lithium, other drugs that can reduce urinary concentrating ability include the following:

  • Amphotericin B
  • Cidofovir
  • Demeclocycline
  • Didanosine
  • Foscarnet
  • Ofloxacin
  • Orlistat

Hereditary nephrogenic DI

Hereditary nephrogenic DI is relatively rare.[3] The most common inherited form results from mutations in the AVP receptor 2 gene (AVPR2) on chromosome Xq28.[19] Defects in the AVP receptor cause resistance to the antidiuretic effect of vasopressin. Because hereditary nephrogenic DI is an X-linked disorder, most cases occur in males; however, cases occasionally arise in females as a result of skewed X inactivation.[20]

Approximately 1% of familial nephrogenic DI cases result from mutations in AQP2 (aquaporin 2), a gene on chromosome 12q13 that gives rise to a water channel that is expressed exclusively in the kidney’s collecting ducts. Autosomal recessive and autosomal dominant forms of nephrogenic DI from AQP2 mutations have been reported.[2]

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Epidemiology

DI is uncommon in the United States, with a prevalence of 3 cases per 100,000 population.[21] No significant sex-related differences in central or nephrogenic DI exist, with male and female prevalence being equal. Similarly, no significant differences in prevalence among ethnic groups have been found.

With both central and nephrogenic DI, inherited causes account for approximately 1-2% of all cases. An incidence of about 1 in 20 million births for nephrogenic DI caused by AQP2 mutations has been cited.[22]

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Prognosis

The prognosis for patients with DI is generally excellent, depending on the underlying illness. In nephrogenic DI caused by medication (eg, lithium), stopping the medication may help to restore normal renal function; after many years of lithium use, however, permanent nephrogenic DI may occur.

DI-related mortality is rare in adults as long as water is available. Severe dehydration, hypernatremia, fever, cardiovascular collapse, and death can ensue in children and elderly people, as well as in persons with complicating illnesses.

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Contributor Information and Disclosures
Author

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Cooperman, MD Clinical Associate Professor of Endocrinology, Temple University School of Medicine; Chair, Department of Internal Medicine, Division of Endocrinology, Jeanes Hospital

Michael Cooperman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Association of Clinical Endocrinologists, Endocrine Society

Disclosure: Nothing to disclose.

Jagdeesh Ullal, MD, MS Assistant Professor of Internal Medicine, Division of Endocrinology, Eastern Virginia Medical School

Jagdeesh Ullal, MD, MS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group

Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, andInternational Society for Clinical Densitometry

Disclosure: Nothing to disclose.

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