Editing Diabetes insipidus

{{Short description|Condition characterized by large amounts of dilute urine and increased thirst}}
{{Distinguish|diabetes mellitus|text=[[diabetes|diabetes mellitus]], commonly shortened to diabetes}}
{{Infobox medical condition (new)
| name            = Diabetes insipidus
| image           = Arginine vasopressin3d.png
| caption         = [[Vasopressin]]
| pronounce       = Diabetes: {{IPAc-en|ˌ|d|aɪ|.|ə|ˈ|b|iː|t|iː|z}} or {{IPAc-en|ˌ|d|aɪ|.|ə|ˈ|b|iː|t|ᵻ|s}}
| field           = [[Endocrinology]]
| symptoms        = Large amounts of dilute urine, increased thirst<ref name=NIH2015/>
| complications   = [[Dehydration]], [[seizure]]s<ref name=NIH2015/>
| onset           = Any age<ref name=NORD2015CDI/><ref name=NORD2016NDI/>
| duration        =
| types         = {{Plainlist|
* AVP-D ([[Central diabetes insipidus|central]])
* AVP-R ([[Nephrogenic diabetes insipidus|nephrogenic]])
* dipsogenic
* gestational<ref name=NIH2015/>}}
| causes          = Depends on the type<ref name=NIH2015/>
| risks           =
| diagnosis       = [[Urine test]]s, [[blood test]]s, [[fluid deprivation test]]<ref name=NIH2015/>
| differential    = [[Diabetes]] mellitus<ref name=NIH2015/>
| prevention      =
| treatment       = Drinking sufficient fluids<ref name=NIH2015/>
| medication      = [[Desmopressin]], [[thiazide]]s, [[aspirin]]<ref name=NIH2015/>
| prognosis       = Good with treatment<ref name=NIH2015/>
| frequency       = 3 per 100,000 per year<ref name=Sab2000/>
| deaths          =
}}

<!-- Definition and symptoms -->
'''Diabetes insipidus''' ('''DI''') is a [[Disease|condition]] characterized by [[Polyuria|large amounts of dilute urine]] and [[Polydipsia|increased thirst]].<ref name="NIH2015">{{Cite web |date=October 2015 |title=Diabetes Insipidus |url=https://www.niddk.nih.gov/health-information/kidney-disease/diabetes-insipidus |url-status=live |archive-url=https://web.archive.org/web/20170513120920/https://www.niddk.nih.gov/health-information/kidney-disease/diabetes-insipidus |archive-date=13 May 2017 |access-date=28 May 2017 |website=National Institute of Diabetes and Digestive and Kidney Diseases}}</ref> The amount of urine produced can be nearly 20 liters per day.<ref name=NIH2015/> Reduction of fluid has little effect on the concentration of the urine.<ref name=NIH2015/> Complications may include [[dehydration]] or [[Epileptic seizure|seizures]].<ref name=NIH2015/>

<!-- Cause and diagnosis -->
There are four types of DI, each with a different set of causes.<ref name=NIH2015/>

# [[Central diabetes insipidus|Central DI]] (CDI), now known as '''arginine vasopressin deficiency''' ('''AVP-D'''),<ref name=":1">{{Cite journal |last=Arima |first=Hiroshi |last2=Bichet |first2=Daniel G. |last3=Cheetham |first3=Timothy |last4=Christ-Crain |first4=Mirjam |last5=Drummond |first5=Juliana |last6=Gurnell |first6=Mark |last7=Levy |first7=Miles |last8=McCormack |first8=Ann |last9=Newell-Price |first9=John |last10=Verbalis |first10=Joseph G. |last11=Wass |first11=John |last12=Cooper |first12=Deborah |date=2022-12-01 |title=Changing the name of diabetes insipidus |url=https://doi.org/10.1007/s11102-022-01276-2 |journal=Pituitary |language=en |volume=25 |issue=6 |pages=777–779 |doi=10.1007/s11102-022-01276-2 |issn=1573-7403 |pmid=36334185 |s2cid=253350878}}</ref> is due to a lack of [[vasopressin]] (antidiuretic hormone) production.<ref name="NIH2015" /> This can be due to injury to the [[hypothalamus]] or [[pituitary gland]] or due to [[genetics]].<ref name="NIH2015" />
# [[Nephrogenic diabetes insipidus|Nephrogenic DI]] (NDI), also known as '''arginine vasopressin resistance''' ('''AVP-R'''),<ref name=":1" /> occurs when the [[kidney]]s do not respond properly to vasopressin.<ref name="NIH2015" />
# Dipsogenic DI is a result of [[Primary polydipsia|excessive fluid intake]] due to damage to the [[Hypothalamus|hypothalamic]] [[thirst]] mechanism.<ref name="NIH2015" /> It occurs more often in those with certain [[psychiatric disorders]] or on certain medications.<ref name="NIH2015" />
# Gestational DI occurs only during [[pregnancy]].<ref name="NIH2015" />

Diagnosis is often based on [[Clinical urine tests|urine tests]], [[blood test]]s and the [[fluid deprivation test]].<ref name="NIH2015" /> Despite the name, 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.<ref name="NIH2015" />

<!-- Treatment, epidemiology and culture-->
Treatment involves drinking sufficient fluids to prevent dehydration.<ref name=NIH2015/> Other treatments depend on the type.<ref name=NIH2015/> In central and gestational DI, treatment is with [[desmopressin]].<ref name=NIH2015/> Nephrogenic DI may be treated by addressing the underlying cause or by the use of a [[thiazide]], [[aspirin]] or [[ibuprofen]].<ref name=NIH2015/> The number of new cases of diabetes insipidus each year is 3 in 100,000.<ref name="Sab2000">{{Cite journal |vauthors=Saborio P, Tipton GA, Chan JC |year=2000 |title=Diabetes Insipidus |journal=Pediatrics in Review |volume=21 |issue=4 |pages=122–129 |doi=10.1542/pir.21-4-122 |pmid=10756175 |s2cid=28020447}}</ref> Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally.<ref name="NORD2015CDI">{{Cite web |date=2015 |title=Central Diabetes Insipidus |url=https://rarediseases.org/rare-diseases/central-diabetes-insipidus/ |url-status=live |archive-url=https://web.archive.org/web/20170221045116/https://rarediseases.org/rare-diseases/central-diabetes-insipidus/ |archive-date=21 February 2017 |access-date=28 May 2017 |website=NORD (National Organization for Rare Disorders)}}</ref> Nephrogenic DI can begin at any age.<ref name="NORD2016NDI">{{Cite web |date=2016 |title=Nephrogenic Diabetes Insipidus |url=https://rarediseases.org/rare-diseases/nephrogenic-diabetes-insipidus/ |url-status=live |archive-url=https://web.archive.org/web/20170219084854/https://rarediseases.org/rare-diseases/nephrogenic-diabetes-insipidus/ |archive-date=19 February 2017 |access-date=28 May 2017 |website=NORD (National Organization for Rare Disorders)}}</ref> The term "diabetes" is derived from the [[Greek language|Greek]] word meaning [[siphon]].<ref name=":0">{{Cite book |url=https://books.google.com/books?id=uYD92j-iQo8C&pg=PA19 |title=Diabetes For Dummies |vauthors=Rubin AL |date=2011 |publisher=John Wiley & Sons |isbn=9781118052488 |edition=3 |page=19 |language=en |archive-url=https://web.archive.org/web/20170908191512/https://books.google.ca/books?id=uYD92j-iQo8C&pg=PA19 |archive-date=2017-09-08 |url-status=live}}</ref>

==Signs and symptoms==
Excessive urination and extreme [[thirst]] and [[polydipsia|increased fluid intake]] (especially for cold water and sometimes ice or ice water) are typical for DI.<ref>{{Cite web |last=USE |title=Diabetes insipidus - PubMed Health |url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001415/ |url-status=live |archive-url=https://web.archive.org/web/20120829121450/http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001415/ |archive-date=2012-08-29 |access-date=2012-05-28 |publisher=Ncbi.nlm.nih.gov}}</ref> 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 properly regulate the amount of the water it takes in.<ref>{{Cite web |last=Watts |first=Mike |date=2019-01-15 |title=Dehydration and Diabetes |url=https://www.diabetes.co.uk/dehydration-and-diabetes.html |access-date=2024-02-01 |website=Diabetes |language=en-GB}}</ref>

Extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain and [[human development (biology)|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|date=October 2021}}<ref>{{Cite web |title=Diabetes Insipidus vs. Diabetes Mellitus |url=https://www.webmd.com/diabetes/diabetes-insipidus-vs-diabetes-mellitus}}</ref>

==Cause==
The several forms of diabetes insipidus are:

===Central===
{{main|Central diabetes insipidus}}

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:{{citation needed|date=September 2024}}
* [[Idiopathic disease|Idiopathic]] – 30% (including autoimmune, genetic, and familial forms)
* Malignant or benign tumors of the brain or pituitary – 25%
* Cranial surgery – 20%
* Head trauma – 16%

===Nephrogenic===
{{main|Nephrogenic diabetes insipidus}}
Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to vasopressin.<ref>{{Cite journal |vauthors=Bichet DG |date=April 2006 |title=Nephrogenic Diabetes Insipidus |journal=Advances in Chronic Kidney Disease |language=en |volume=13 |issue=2 |pages=96–104 |doi=10.1053/j.ackd.2006.01.006 |pmid=16580609}}</ref>

===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]],<ref name="pmid16544179">{{Cite journal |vauthors=Perkins RM, Yuan CM, Welch PG |date=March 2006 |title=Dipsogenic diabetes insipidus: report of a novel treatment strategy and literature review |journal=Clin. Exp. Nephrol. |volume=10 |issue=1 |pages=63–7 |doi=10.1007/s10157-005-0397-0 |pmid=16544179 |s2cid=6874287}}</ref> or due to mental illness. Treatment with desmopressin may lead to [[water intoxication]].<ref>{{Cite web |date=31 October 2017 |title=Diabetes insipidus |url=https://www.nhs.uk/conditions/diabetes-insipidus/treatment/}}</ref>

===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.<ref name="pmid17308961">{{Cite journal |vauthors=Kalelioglu I, Kubat Uzum A, Yildirim A, Ozkan T, Gungor F, Has R |year=2007 |title=Transient gestational diabetes insipidus diagnosed in successive pregnancies: review of pathophysiology, diagnosis, treatment, and management of delivery |journal=Pituitary |volume=10 |issue=1 |pages=87–93 |doi=10.1007/s11102-007-0006-1 |pmid=17308961 |s2cid=9493532}}</ref>

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.<ref>{{Cite journal |last=Ananthakrishnan |first=Sonia |date=March 2016 |title=Diabetes insipidus during pregnancy |journal=Best Practice & Research Clinical Endocrinology & Metabolism |volume=30 |issue=2 |pages=305–315 |doi=10.1016/j.beem.2016.02.005 |pmid=27156766}}</ref>

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.{{citation needed|date=September 2024}}

==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.<ref>{{Cite journal |last=Watson |first=Fiona |last2=Austin |first2=Pauline |date=2021-10-01 |title=Physiology of human fluid balance |url=https://www.sciencedirect.com/science/article/pii/S1472029921001818 |journal=Anaesthesia & Intensive Care Medicine |language=en |volume=22 |issue=10 |pages=644–651 |doi=10.1016/j.mpaic.2021.07.010 |issn=1472-0299}}</ref>

The regulation of urine production occurs in the [[hypothalamus]], which produces [[Vasopressin|ADH]] in the [[Supraoptic nucleus|supraoptic]] and [[Paraventricular nucleus|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 [[Cerebral cortex|cortex]].{{citation needed|date=April 2022}}

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|date=October 2021}}

The main effector organ for [[body water|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 [[aquaporin]]s 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.{{citation needed|date=September 2024}}

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]], [[Hypercalcaemia|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.{{citation needed|date=September 2024}}

Hereditary forms of diabetes insipidus account for less than 10% of the cases of diabetes insipidus seen in clinical practice.<ref>{{Cite journal |vauthors=Fujiwara TM, Bichet DG |year=2005 |title=Molecular Biology of Hereditary Diabetes Insipidus |journal=Journal of the American Society of Nephrology |volume=16 |issue=10 |pages=2836–2846 |doi=10.1681/ASN.2005040371 |pmid=16093448 |doi-access=free}}</ref>

==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 [[electrolyte]]s 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.<ref>{{Cite journal |vauthors=Kamel KS, Halperin ML |date=May 2021 |title=Use of Urine Electrolytes and Urine Osmolality in the Clinical Diagnosis of Fluid, Electrolytes, and Acid-Base Disorders |journal=Kidney International Reports |language=English |volume=6 |issue=5 |pages=1211–1224 |doi=10.1016/j.ekir.2021.02.003 |pmc=8116912 |pmid=34013099}}</ref>

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:{{citation needed|date=September 2024}}
# a defect in [[antidiuretic hormone|ADH]] production
# 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.<ref name=agabegi2nd/> 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.<ref name="agabegi2nd">{{Cite book |last=Elizabeth D Agabegi |url=https://archive.org/details/stepuptomedicine0000agab |title=Step-Up to Medicine (Step-Up Series) |last2=Agabegi, Steven S. |publisher=Lippincott Williams & Wilkins |year=2008 |isbn=978-0-7817-7153-5 |location=Hagerstwon, MD |url-access=registration}}</ref> Sometimes measuring blood levels of ADH toward the end of this test is also necessary, but is more time-consuming to perform.<ref name=agabegi2nd/>

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|date=August 2019}}

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<ref name="pmid17371462">{{Cite journal |vauthors=Crowley RK, Sherlock M, Agha A, Smith D, Thompson CJ |year=2007 |title=Clinical insights into adipsic diabetes insipidus: a large case series |journal=Clin. Endocrinol. |volume=66 |issue=4 |pages=475–82 |doi=10.1111/j.1365-2265.2007.02754.x |pmid=17371462 |s2cid=28845882}}</ref> as a marked absence of thirst even in response to hyperosmolality.<ref name="pmid21301966">{{Cite journal |vauthors=Sinha A, Ball S, Jenkins A, Hale J, Cheetham T |year=2011 |title=Objective assessment of thirst recovery in patients with adipsic diabetes insipidus |journal=Pituitary |volume=14 |issue=4 |pages=307–11 |doi=10.1007/s11102-011-0294-3 |pmid=21301966 |s2cid=25062519}}</ref> In some cases of adipsic DI, the person may also fail to respond to desmopressin.<ref name="pmid12364435">{{Cite journal |vauthors=Smith D, McKenna K, Moore K, Tormey W, Finucane J, Phillips J, Baylis P, Thompson CJ |year=2002 |title=Baroregulation of vasopressin release in adipsic diabetes insipidus |journal=J. Clin. Endocrinol. Metab. |volume=87 |issue=10 |pages=4564–8 |doi=10.1210/jc.2002-020090 |pmid=12364435 |doi-access=free}}</ref>

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|date=August 2019}}

==Treatment==
Treatment involves drinking sufficient fluids to prevent dehydration.<ref name=NIH2015/> Other treatments depend on the type.<ref name=NIH2015/> In central and gestational DI treatment is with [[desmopressin]].<ref name=NIH2015/> Nephrogenic DI may be treated by addressing the underlying cause or the use of a [[thiazide]], [[aspirin]], or [[ibuprofen]].<ref name=NIH2015/>

===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.{{citation needed|date=September 2024}}

===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.<ref>{{Cite journal |vauthors=Verbalis JG |date=May 2003 |title=Diabetes insipidus |journal=Rev Endocr Metab Disord |volume=4 |issue=2 |pages=177–85 |doi=10.1023/A:1022946220908 |pmid=12766546 |s2cid=33533827}}</ref> [[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.<ref>{{Cite journal |last=Loffing J |date=November 2004 |title=Paradoxical antidiuretic effect of thiazides in diabetes insipidus: another piece in the puzzle |url=http://jasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=15504949 |journal=J. Am. Soc. Nephrol. |volume=15 |issue=11 |pages=2948–50 |doi=10.1097/01.ASN.0000146568.82353.04 |pmid=15504949 |doi-access=free}}</ref>

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.<ref>{{Cite journal |vauthors=Finch CK, Kelley KW, Williams RB |date=April 2003 |title=Treatment of lithium-induced diabetes insipidus with amiloride |journal=Pharmacotherapy |volume=23 |issue=4 |pages=546–50 |doi=10.1592/phco.23.4.546.32121 |pmid=12680486 |s2cid=28291646}}</ref>

== Etymology ==
The word "diabetes" ({{IPAc-en|ˌ|d|aɪ|.|ə|ˈ|b|iː|t|iː|z}} or {{IPAc-en|ˌ|d|aɪ|.|ə|ˈ|b|iː|t|ᵻ|s}}) comes from [[Latin]] {{Lang|la|diabētēs}}, which in turn comes from {{Langx|grc|διαβήτης|translit=diabētēs}}, which literally means "a passer through; a [[siphon]]".<ref name="OED_diabetes">Oxford English Dictionary. ''diabetes''. Retrieved 2011-06-10.</ref> [[Ancient Greece|Ancient Greek]] [[physician]] [[Aretaeus of Cappadocia]] ([[Floruit|fl.]] in the first century [[Common Era|CE]]) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.<ref name="OnlineEtymology_diabetes">{{Cite web |year=2001–2010 |title=Online Etymology Dictionary. ''diabetes.'' |url=http://www.etymonline.com/index.php?search=diabetes&searchmode=none |url-status=live |archive-url=https://web.archive.org/web/20120113074242/http://www.etymonline.com/index.php?search=diabetes&searchmode=none |archive-date=2012-01-13 |access-date=2011-06-10 |vauthors=Harper D}}</ref><ref name="RCPE">{{Cite web |year=2011 |title=Royal College of Physicians of Edinburgh. Diabetes, Doctors and Dogs: An exhibition on Diabetes and Endocrinology by the College Library for the 43rd St. Andrew's Day Festival Symposium |url=http://www.rcpe.ac.uk/library/exhibitions/diabetes/ |archive-url=https://web.archive.org/web/20110927133910/http://www.rcpe.ac.uk/library/exhibitions/diabetes/ |archive-date=2011-09-27 |access-date=2019-01-14 |vauthors=Dallas J}}</ref> Ultimately, the word comes from Greek {{Lang|grc|διαβαίνειν}} ({{Transliteration|grc|diabainein}}), meaning "to pass through",<ref name="OED_diabetes" /> which is composed of {{Lang|grc|δια}}- (''dia''-), meaning "through" and {{Lang|grc|βαίνειν}} ({{Transliteration|grc|bainein}}), meaning "to go".<ref name="OnlineEtymology_diabetes" /> The word "diabetes" is first recorded in English, in the form "diabete", in a medical text written around 1425.

"Insipidus" comes from Latin language {{Lang|la|insipidus}} (tasteless), from Latin: ''in-'' "not" + {{Lang|la|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.<ref name=":0" />

== See also ==
* [[Diabetes mellitus]]
* [[Polyuria]]
* [[Polydipsia]]

==References==
{{Reflist}}

== External links ==

{{Pituitary disease}}
{{Nephrology}}
{{X-linked disorders}}
{{Medical resources
| oMIM_mult       = {{OMIM2|125800}}
| medlinePlus_mult= <br />Central{{MedlinePlus2|000460}}<br />Congenital{{MedlinePlus2|000461}}<br />Nephrogenic {{MedlinePlus2|000511}}
|  DiseasesDB     = 3639
|  ICD11          = {{ICD11|5A61.5}} {{ICD11|GB90.4A}}
|  ICD10          = {{ICD10|E|23|2|e|20}} {{ICD10|N|25|1|n|25}}
|  ICD9           = {{ICD9|253.5}} {{ICD9|588.1}}
|  ICDO           =
|  OMIM           = 304800
|  MedlinePlus    = 000377
|  eMedicineSubj  = med
|  eMedicineTopic = 543
|  eMedicine_mult = {{eMedicine2|ped|580}}
|  MeshID         = D003919
}}
{{Authority control}}

{{DEFAULTSORT:Diabetes Insipidus}}
[[Category:Endocrine diseases]]
[[Category:Nephrology]]
[[Category:Rare diseases]]
[[Category:Thirst]]
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[[Category:Wikipedia neurology articles ready to translate]]