Diabetes insipidus

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Diabetes insipidus
Arginine vasopressin3d.png
Vasopressin
Pronunciation
Specialty Endocrinology
Symptoms Large amounts of dilute urine, increased thirst [1]
Complications Dehydration, seizures [1]
Usual onsetAny age [2] [3]
TypesCentral, nephrogenic, dipsogenic, gestational [1]
CausesDepends on the type [1]
Diagnostic method Urine tests, blood tests, fluid deprivation test [1]
Differential diagnosis Diabetes mellitus [1]
TreatmentDrinking sufficient fluids [1]
Medication Desmopressin, thiazides, aspirin [1]
Prognosis Good with treatment [1]
Frequency3 per 100,000 per year [4]

Diabetes insipidus (DI), alternately called arginine vasopressin deficiency (AVP-D) or arginine vasopressin resistance (AVP-R), [5] is a condition characterized by large amounts of dilute urine and increased thirst. [1] The amount of urine produced can be nearly 20 liters per day. [1] Reduction of fluid has little effect on the concentration of the urine. [1] Complications may include dehydration or seizures. [1]

Contents

There are four types of DI, each with a different set of causes. [1] Central DI (CDI) is due to a lack of vasopressin (antidiuretic hormone) production. [1] This can be due to injury to the hypothalamus or pituitary gland or genetics. [1] Nephrogenic DI (NDI) occurs when the kidneys do not respond properly to vasopressin. [1] Dipsogenic DI is a result of excessive fluid intake due to damage to the hypothalamic thirst mechanism. [1] It occurs more often in those with certain psychiatric disorders or on certain medications. [1] Gestational DI occurs only during pregnancy. [1] Diagnosis is often based on urine tests, blood tests and the fluid deprivation test. [1] Diabetes insipidus is unrelated to diabetes mellitus and the conditions have a distinct mechanism, though both can result in the production of large amounts of urine. [1]

Treatment involves drinking sufficient fluids to prevent dehydration. [1] Other treatments depend on the type. [1] In central and gestational DI, treatment is with desmopressin. [1] Nephrogenic DI may be treated by addressing the underlying cause or by the use of a thiazide, aspirin or ibuprofen. [1] The number of new cases of diabetes insipidus each year is 3 in 100,000. [4] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally. [2] Nephrogenic DI can begin at any age. [3] The term "diabetes" is derived from the Greek word meaning siphon. [6]

Signs and symptoms

Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI. [7] The symptoms of excessive urination and extreme thirst are similar to what is seen in untreated diabetes mellitus, with the distinction that the urine does not contain glucose. Blurred vision is a rarity. Signs of dehydration may also appear in some individuals since the body cannot conserve much (if any) of the water it takes in.[ citation needed ]

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 consumed to offset the urinary losses. However, there is a continuous risk of dehydration and loss of potassium that may lead to hypokalemia.[ citation needed ] [8]

Cause

The several forms of diabetes insipidus are:

Central

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

Nephrogenic

Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to vasopressin. [9]

Dipsogenic

Dipsogenic DI or primary polydipsia results from excessive intake of fluids as opposed to deficiency of arginine vasopressin. It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus, [10] or due to mental illness. Treatment with desmopressin may lead to water intoxication. [11]

Gestational

Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down antidiuretic hormone (ADH). Gestational DI is thought to occur with excessive production and/or impaired clearance of vasopressinase. [12]

Most cases of gestational DI can be treated with desmopressin (DDAVP), but not vasopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used. [13]

Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver of pregnancy. These cause DI by impairing hepatic clearance of circulating vasopressinase.

Pathophysiology

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. [14]

The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.[ citation needed ]

Neurogenic/central DI results from a lack of ADH; occasionally it can present with decreased thirst as regulation of thirst and ADH production occur in close proximity in the hypothalamus. It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without an underlying cause (idiopathic).[ citation needed ]

The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules; specifically, it acts on proteins called aquaporins and more specifically aquaporin 2 in the following cascade. When released, ADH binds to V2 G-protein coupled receptors within the distal convoluted tubules, increasing cyclic AMP, which couples with protein kinase A, stimulating translocation of the aquaporin 2 channel stored in the cytoplasm of the distal convoluted tubules and collecting ducts into the apical membrane. These transcribed channels allow water into the collecting duct cells. The increase in permeability allows for the reabsorption of water into the bloodstream, thus concentrating the urine.

Nephrogenic DI results from a lack of aquaporin channels in the distal collecting duct (decreased surface expression and transcription). It is seen in lithium toxicity, hypercalcemia, hypokalemia, or the release of ureteral obstruction. Therefore, a lack of ADH prevents water reabsorption and the osmolarity of the blood increases. With increased osmolarity, the osmoreceptors in the hypothalamus detect this change and stimulate thirst. With increased thirst, the person now experiences a polydipsia and polyuria cycle.

Hereditary forms of diabetes insipidus account for less than 10% of the cases of diabetes insipidus seen in clinical practice. [15]

Diagnosis

To distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops). Urinalysis demonstrates a dilute urine with a low specific gravity. Urine osmolarity and electrolyte levels are typically low. [16]

A fluid deprivation test is another way of distinguishing DI from other causes of excessive urination. If there is no change in fluid loss, giving desmopressin can determine if DI is caused by:

  1. a defect in ADH production
  2. a defect in the kidneys' response to ADH

This test measures the changes in body weight, urine output, and urine composition when fluids are withheld to induce dehydration. The body's normal response to dehydration is to conserve water by concentrating the urine. Those with DI continue to urinate large amounts of dilute urine in spite of water deprivation. In primary polydipsia, the urine osmolality should increase and stabilize at above 280 mOsm/kg with fluid restriction, while a stabilization at a lower level indicates diabetes insipidus. [17] Stabilization in this test means, more specifically, when the increase in urine osmolality is less than 30 Osm/kg per hour for at least three hours. [17] Sometimes measuring blood levels of ADH toward the end of this test is also necessary, but is more time-consuming to perform. [17]

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 person should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in the central nervous system. If desmopressin reduces urine output and increases urine osmolarity, the hypothalamic production of ADH is deficient, and the kidney responds normally to exogenous vasopressin (desmopressin). If the DI is due to kidney pathology, desmopressin does not change either urine output or osmolarity (since the endogenous vasopressin levels are already high).[ medical citation needed ]

Whilst diabetes insipidus usually occurs with polydipsia, it can also rarely occur not only in the absence of polydipsia but in the presence of its opposite, adipsia (or hypodipsia). "Adipsic diabetes insipidus" is recognised [18] as a marked absence of thirst even in response to hyperosmolality. [19] In some cases of adipsic DI, the person may also fail to respond to desmopressin. [20]

If central DI is suspected, testing of other hormones of the pituitary, as well as magnetic resonance imaging, particularly a pituitary MRI, is necessary to discover if a disease process (such as a prolactinoma, or histiocytosis, syphilis, tuberculosis or other tumor or granuloma) is affecting pituitary function. Most people with this form have either experienced past head trauma or have stopped ADH production for an unknown reason.[ medical citation needed ]

Treatment

Treatment involves drinking sufficient fluids to prevent dehydration. [1] Other treatments depend on the type. [1] In central and gestational DI treatment is with desmopressin. [1] Nephrogenic DI may be treated by addressing the underlying cause or the use of a thiazide, aspirin, or ibuprofen. [1]

Central

Central DI and gestational DI respond to desmopressin which is given as intranasal or oral tablets. Carbamazepine, an anticonvulsive medication, has also had some success in this type of DI. Also, gestational DI tends to abate on its own in four to six weeks following labor, though some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is not usually an option.

Nephrogenic

Desmopressin will be ineffective in nephrogenic DI which is treated by reversing the underlying cause (if possible) and replacing the free water deficit. A thiazide diuretic, such as chlorthalidone or hydrochlorothiazide, can be used to create mild hypovolemia which encourages salt and water uptake in proximal tubule and thus improve nephrogenic diabetes insipidus. [21] Amiloride has additional benefit of blocking Na uptake. Thiazide diuretics are sometimes combined with amiloride to prevent hypokalemia caused by the thiazides. It seems paradoxical to treat an extreme diuresis with a diuretic, and the exact mechanism of action is unknown but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering the glomerular filtration rate and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained. [22]

Lithium-induced nephrogenic DI may be effectively managed with the administration of amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics. Clinicians have been aware of lithium toxicity for many years, and traditionally have administered thiazide diuretics for lithium-induced polyuria and nephrogenic diabetes insipidus. However, amiloride has recently been shown to be a successful treatment for this condition. [23]

Etymology

The word "diabetes" ( /ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɪs/ ) comes from Latin diabētēs, which in turn comes from Ancient Greek : διαβήτης, romanized: diabētēs, which literally means "a passer through; a siphon". [24] Ancient Greek physician Aretaeus of Cappadocia (fl. in the first century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. [25] [26] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", [24] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". [25] The word "diabetes" is first recorded in English, in the form "diabete", in a medical text written around 1425.

"Insipidus" comes from Latin language insipidus (tasteless), from Latin: in- "not" + sapidus "tasty" from sapere "have a taste"—the full meaning is "lacking flavor or zest; not tasty". Application of this name to DI arose from the fact that diabetes insipidus does not cause glycosuria (excretion of glucose into the urine).

In a large survey conducted amongst patients with central diabetes insipidus, the majority were in favor of changing the disease's name to "vasopressin deficiency" to avoid confusion with diabetes mellitus. [6]

Related Research Articles

Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. Symptoms can be absent, mild or severe. Mild symptoms include a decreased ability to think, headaches, nausea, and poor balance. Severe symptoms include confusion, seizures, and coma; death can ensue.

<span class="mw-page-title-main">Vasopressin</span> Mammalian hormone released from the pituitary gland

Human vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized from the AVP gene as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon terminating in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular fluid hypertonicity (hyperosmolality). AVP has two primary functions. First, it increases the amount of solute-free water reabsorbed back into the circulation from the filtrate in the kidney tubules of the nephrons. Second, AVP constricts arterioles, which increases peripheral vascular resistance and raises arterial blood pressure.

Diuresis is the excretion of urine, especially when excessive (polyuria). The term collectively denotes the physiologic processes underpinning increased urine production by the kidneys during maintenance of fluid balance.

<span class="mw-page-title-main">Desmopressin</span> Medication

Desmopressin, sold under the trade name DDAVP among others, is a medication used to treat diabetes insipidus, bedwetting, hemophilia A, von Willebrand disease, and high blood urea levels. In hemophilia A and von Willebrand disease, it should only be used for mild to moderate cases. It may be given in the nose, by injection into a vein, by mouth, or under the tongue.

Hypernatremia, also spelled hypernatraemia, is a high concentration of sodium in the blood. Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite. Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain. Normal serum sodium levels are 135–145 mmol/L. Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L. Severe symptoms typically only occur when levels are above 160 mmol/L.

The Syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD), is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes a physiologically inappropriate increase in solute-free water being reabsorbed by the tubules of the kidney to the venous circulation leading to hypotonic hyponatremia.

<span class="mw-page-title-main">Chlortalidone</span> Thiazide-like diuretic drug

Chlortalidone, also known as chlorthalidone, is a thiazide-like diuretic drug used to treat high blood pressure, swelling, diabetes insipidus, and renal tubular acidosis. Because chlortalidone is effective in most patients with high blood pressure, it is considered a preferred initial treatment. It is also used to prevent calcium-based kidney stones. It is taken by mouth. Effects generally begin within three hours and last for up to three days. Long-term treatment with chlortalidone is more effective than hydrochlorothiazide for prevention of heart attack or stroke.

Fluid balance is an aspect of the homeostasis of organisms in which the amount of water in the organism needs to be controlled, via osmoregulation and behavior, such that the concentrations of electrolytes in the various body fluids are kept within healthy ranges. The core principle of fluid balance is that the amount of water lost from the body must equal the amount of water taken in; for example, in humans, the output must equal the input. Euvolemia is the state of normal body fluid volume, including blood volume, interstitial fluid volume, and intracellular fluid volume; hypovolemia and hypervolemia are imbalances. Water is necessary for all life on Earth. Humans can survive for 4 to 6 weeks without food but only for a few days without water.

Nocturia is defined by the International Continence Society (ICS) as “the complaint that the individual has to wake at night one or more times for voiding .” The term is derived from Latin nox, night, and Greek [τα] ούρα, urine. Causes are varied and can be difficult to discern. Although not every patient needs treatment, most people seek treatment for severe nocturia, waking up to void more than 2–3 times per night.

Nephrogenic diabetes insipidus,, is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central or neurogenic diabetes insipidus, which is caused by insufficient levels of vasopressin. Nephrogenic diabetes insipidus is caused by an improper response of the kidney to vasopressin, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water.

<span class="mw-page-title-main">Primary polydipsia</span> Medical condition

Primary polydipsia and psychogenic polydipsia are forms of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink. Psychogenic polydipsia which is caused by psychiatric disorders, often schizophrenia, is often accompanied by the sensation of dry mouth. Some forms of polydipsia are explicitly non-psychogenic. Primary polydipsia is a diagnosis of exclusion.

<span class="mw-page-title-main">Vasopressin receptor 2</span> Protein-coding gene in the species Homo sapiens

Vasopressin receptor 2 (V2R), or arginine vasopressin receptor 2, is a protein that acts as receptor for vasopressin. AVPR2 belongs to the subfamily of G-protein-coupled receptors. Its activity is mediated by the Gs type of G proteins, which stimulate adenylate cyclase.

<span class="mw-page-title-main">Aquaporin-2</span> Protein-coding gene in the species Homo sapiens

Aquaporin-2 (AQP-2) is found in the apical cell membranes of the kidney's collecting duct principal cells and in intracellular vesicles located throughout the cell. It is encoded by the AQP2 gene.

<span class="mw-page-title-main">Fluid deprivation test</span>

A fluid or water deprivation test is a medical test which can be used to determine whether the patient has diabetes insipidus as opposed to other causes of polydipsia. The patient is required, for a prolonged period, to forgo intake of water completely, to determine the cause of the thirst.

An antidiuretic is a substance that helps to control fluid balance in an animal's body by reducing urination, opposing diuresis. Its effects are opposite that of a diuretic. The major endogenous antidiuretics are antidiuretic hormone and oxytocin. Both of those are also used exogenously as medications in people whose bodies need extra help with fluid balance via suppression of diuresis. In addition, there are various other antidiuretic drugs, some molecularly close to ADH or oxytocin and others not. Antidiuretics reduce urine volume, particularly in diabetes insipidus (DI), which is one of their main indications.

Central diabetes insipidus, has now been renamed Arginine Vasopressin Deficiency because of a fatal confusion of the condition with diabetes mellitus. https://www.pituitary.org.uk/diabetes-insipidus-is-changing-its-name-arginine-vasopressin-deficiency/.

Hypothalamic disease is a disorder presenting primarily in the hypothalamus, which may be caused by damage resulting from malnutrition, including anorexia and bulimia eating disorders, genetic disorders, radiation, surgery, head trauma, lesion, tumour or other physical injury to the hypothalamus. The hypothalamus is the control center for several endocrine functions. Endocrine systems controlled by the hypothalamus are regulated by antidiuretic hormone (ADH), corticotropin-releasing hormone, gonadotropin-releasing hormone, growth hormone-releasing hormone, oxytocin, all of which are secreted by the hypothalamus. Damage to the hypothalamus may impact any of these hormones and the related endocrine systems. Many of these hypothalamic hormones act on the pituitary gland. Hypothalamic disease therefore affects the functioning of the pituitary and the target organs controlled by the pituitary, including the adrenal glands, ovaries and testes, and the thyroid gland.

Hypoosmolar hyponatremia is a condition where hyponatremia is associated with a low plasma osmolality. The term "hypotonic hyponatremia" is also sometimes used.

<span class="mw-page-title-main">Adipsia</span> Medical condition

Adipsia, also known as hypodipsia, is a symptom of inappropriately decreased or absent feelings of thirst. It involves an increased osmolality or concentration of solute in the urine, which stimulates secretion of antidiuretic hormone (ADH) from the hypothalamus to the kidneys. This causes the person to retain water and ultimately become unable to feel thirst. Due to its rarity, the disorder has not been the subject of many research studies.

<span class="mw-page-title-main">Diuretic</span> Substance that promotes the production of urine

A diuretic is any substance that promotes diuresis, the increased production of urine. This includes forced diuresis. A diuretic tablet is sometimes colloquially called a water tablet. There are several categories of diuretics. All diuretics increase the excretion of water from the body, through the kidneys. There exist several classes of diuretic, and each works in a distinct way. Alternatively, an antidiuretic, such as vasopressin, is an agent or drug which reduces the excretion of water in urine.

References

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  2. 1 2 "Central Diabetes Insipidus". NORD (National Organization for Rare Disorders). 2015. Archived from the original on 21 February 2017. Retrieved 28 May 2017.
  3. 1 2 "Nephrogenic Diabetes Insipidus". NORD (National Organization for Rare Disorders). 2016. Archived from the original on 19 February 2017. Retrieved 28 May 2017.
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  5. ↑ Arima, Hiroshi; Bichet, Daniel G.; Cheetham, Timothy; Christ-Crain, Mirjam; Drummond, Juliana; Gurnell, Mark; Levy, Miles; McCormack, Ann; Newell-Price, John; Verbalis, Joseph G.; Wass, John; Cooper, Deborah (2022-12-01). "Changing the name of diabetes insipidus". Pituitary. 25 (6): 777–779. doi:10.1007/s11102-022-01276-2. ISSN   1573-7403. PMID   36334185. S2CID   253350878.
  6. 1 2 Rubin AL (2011). Diabetes For Dummies (3 ed.). John Wiley & Sons. p. 19. ISBN   9781118052488. Archived from the original on 2017-09-08.
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  8. ↑ "Diabetes Insipidus vs. Diabetes Mellitus".
  9. ↑ Bichet DG (April 2006). "Nephrogenic Diabetes Insipidus". Advances in Chronic Kidney Disease. 13 (2): 96–104. doi:10.1053/j.ackd.2006.01.006. PMID   16580609.
  10. ↑ Perkins RM, Yuan CM, Welch PG (March 2006). "Dipsogenic diabetes insipidus: report of a novel treatment strategy and literature review". Clin. Exp. Nephrol. 10 (1): 63–7. doi:10.1007/s10157-005-0397-0. PMID   16544179. S2CID   6874287.
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  13. ↑ Ananthakrishnan, Sonia (March 2016). "Diabetes insipidus during pregnancy". Best Practice & Research Clinical Endocrinology & Metabolism. 30 (2): 305–315. doi:10.1016/j.beem.2016.02.005. PMID   27156766.
  14. ↑ Watson, Fiona; Austin, Pauline (2021-10-01). "Physiology of human fluid balance". Anaesthesia & Intensive Care Medicine. 22 (10): 644–651. doi:10.1016/j.mpaic.2021.07.010. ISSN   1472-0299.
  15. ↑ Fujiwara TM, Bichet DG (2005). "Molecular Biology of Hereditary Diabetes Insipidus". Journal of the American Society of Nephrology. 16 (10): 2836–2846. doi: 10.1681/ASN.2005040371 . PMID   16093448.
  16. ↑ Kamel KS, Halperin ML (May 2021). "Use of Urine Electrolytes and Urine Osmolality in the Clinical Diagnosis of Fluid, Electrolytes, and Acid-Base Disorders". Kidney International Reports. 6 (5): 1211–1224. doi:10.1016/j.ekir.2021.02.003. PMC   8116912 . PMID   34013099.
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  22. ↑ Loffing J (November 2004). "Paradoxical antidiuretic effect of thiazides in diabetes insipidus: another piece in the puzzle". J. Am. Soc. Nephrol. 15 (11): 2948–50. doi: 10.1097/01.ASN.0000146568.82353.04 . PMID   15504949.
  23. ↑ Finch CK, Kelley KW, Williams RB (April 2003). "Treatment of lithium-induced diabetes insipidus with amiloride". Pharmacotherapy. 23 (4): 546–50. doi:10.1592/phco.23.4.546.32121. PMID   12680486. S2CID   28291646.
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