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==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=1211β1224 |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=475β82 |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=307β11 |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=4564β8 |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}}
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