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| __NOTOC__ | | __NOTOC__ |
| {{Diabetes insipidus}} | | {{Diabetes insipidus}} |
| {{CMG}} | | {{CMG}}; {{AE}} {{DAMI}} |
| ==Overview== | | ==Overview== |
| Diabetes Insipidus can be classified into central and nephrogenic diabetes insipidus based on the response of the body to administration of desmopressin (DDAVP). It can also be classified based on the levels of ADH present in the body and the levels of hypo- or hypernatremia. | | [[Diabetes insipidus]] can be classified into three types: [[central diabetes insipidus|central]], [[nephrogenic diabetes insipidus|nephrogenic]], and [[psychogenic]] diabetes insipidus. Some rare forms of the disease include [[Gestational age|gestational]] [[diabetes insipidus]], which occurs only in [[pregnancy]], and [[autoimmune]] diabetes insipidus, which is caused by an [[autoimmune]] reaction. |
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| == Classification == | | ==Classification== |
| Classification into central vs nephrogenic DI
| | ==='''[[Central diabetes insipidus|Central DI]]'''=== |
| | *[[CDI]] is caused by the destruction or degeneration of [[neurons]] originating in the [[Supraoptic nucleus|supraoptic]] and [[Paraventricular nucleus|paraventricular nuclei]], which disrupts the normal storage and release of [[ADH]]. |
| | *The most common cause of [[central diabetes insipidus]] ([[CDI]]) is [[idiopathic]] [[diabetes insipidus]] (DI), which accounts for the vast majority of cases of CDI.<ref name="pmid6640507">{{cite journal| author=Kimmel DW, O'Neill BP| title=Systemic cancer presenting as diabetes insipidus. Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus. | journal=Cancer | year= 1983 | volume= 52 | issue= 12 | pages= 2355-8 | pmid=6640507 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6640507 }} </ref><ref name="pmid11018166">{{cite journal| author=Maghnie M, Cosi G, Genovese E, Manca-Bitti ML, Cohen A, Zecca S et al.| title=Central diabetes insipidus in children and young adults. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 14 | pages= 998-1007 | pmid=11018166 | doi=10.1056/NEJM200010053431403 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11018166 }} </ref> |
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| '''Central DI''' | | ==='''[[Nephrogenic diabetes insipidus|Nephrogenic DI]]'''=== |
| | *The most common causes of [[ADH]] resistance severe enough to produce [[polyuria]] are hereditary nephrogenic DI (in children) and chronic [[lithium]] ingestion and [[hypercalcemia]] (in adults). |
| | *Acquired causes are often partially reversible with cessation of the offending drug or correction of [[hypercalcemia]].<ref name="pmid10477148">{{cite journal| author=van Lieburg AF, Knoers NV, Monnens LA| title=Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 9 | pages= 1958-64 | pmid=10477148 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10477148 }} </ref><ref name="pmid15004257">{{cite journal| author=Sasaki S| title=Nephrogenic diabetes insipidus: update of genetic and clinical aspects. | journal=Nephrol Dial Transplant | year= 2004 | volume= 19 | issue= 6 | pages= 1351-3 | pmid=15004257 | doi=10.1093/ndt/gfh172 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15004257 }} </ref><ref name="pmid3037155">{{cite journal| author=Berl T| title=The cAMP system in vasopressin-sensitive nephron segments of the vitamin D-treated rat. | journal=Kidney Int | year= 1987 | volume= 31 | issue= 5 | pages= 1065-71 | pmid=3037155 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3037155 }} </ref> |
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| CDI is caused by the destruction or degeneration of neurons originating in the supraoptic and paraventricular nuclei. Central DI, results from damage to the [[pituitary gland]], which disrupts the normal storage and release of ADH. The most common cause of central diabetes insipidus (CDI), accounting for the vast majority of cases, are idiopathic diabetes insipidus (DI)<ref name="pmid6640507">{{cite journal| author=Kimmel DW, O'Neill BP| title=Systemic cancer presenting as diabetes insipidus. Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus. | journal=Cancer | year= 1983 | volume= 52 | issue= 12 | pages= 2355-8 | pmid=6640507 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6640507 }} </ref><ref name="pmid11018166">{{cite journal| author=Maghnie M, Cosi G, Genovese E, Manca-Bitti ML, Cohen A, Zecca S et al.| title=Central diabetes insipidus in children and young adults. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 14 | pages= 998-1007 | pmid=11018166 | doi=10.1056/NEJM200010053431403 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11018166 }} </ref>. Others include<ref name="pmid11018166">{{cite journal| author=Maghnie M, Cosi G, Genovese E, Manca-Bitti ML, Cohen A, Zecca S et al.| title=Central diabetes insipidus in children and young adults. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 14 | pages= 998-1007 | pmid=11018166 | doi=10.1056/NEJM200010053431403 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11018166 }} </ref>;
| | ==='''Psychogenic Diabetes Insipidus'''=== |
| *Familial and congenital disease
| | *This type of [[DI]] is characterized primarily by excessive water intake. This disorder is most often observed among young women and mentally unstable patients with [[Psychiatric illness|psychiatric illnesses]], including those taking a [[phenothiazine]], which can lead to the sensation of a dry mouth.<ref name="pmid15153548">{{cite journal| author=Devonald MA, Karet FE| title=Renal epithelial traffic jams and one-way streets. | journal=J Am Soc Nephrol | year= 2004 | volume= 15 | issue= 6 | pages= 1370-81 | pmid=15153548 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15153548 }} </ref> |
| **Familial CDI<ref name="pmid11427695">{{cite journal| author=Burbach JP, Luckman SM, Murphy D, Gainer H| title=Gene regulation in the magnocellular hypothalamo-neurohypophysial system. | journal=Physiol Rev | year= 2001 | volume= 81 | issue= 3 | pages= 1197-267 | pmid=11427695 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11427695 }} </ref>
| | *Other identifiable causes of psychogenic diabetes insipidus include [[sarcoidosis]] and [[lesions]] to the [[Hypothalamic pituitary adrenal axis|hypothalamic pituitary axis]], which may disrupt the thirst center, thereby increasing the sensation of [[thirst]] and water consumption.<ref name="pmid9329382">{{cite journal| author=Nomura Y, Onigata K, Nagashima T, Yutani S, Mochizuki H, Nagashima K et al.| title=Detection of skewed X-inactivation in two female carriers of vasopressin type 2 receptor gene mutation. | journal=J Clin Endocrinol Metab | year= 1997 | volume= 82 | issue= 10 | pages= 3434-7 | pmid=9329382 | doi=10.1210/jcem.82.10.4312 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9329382 }} </ref> |
| **Wolfram syndrome also known as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness)<ref name="pmid26025012">{{cite journal| author=Bischoff AN, Reiersen AM, Buttlaire A, Al-Lozi A, Doty T, Marshall BA et al.| title=Selective cognitive and psychiatric manifestations in Wolfram Syndrome. | journal=Orphanet J Rare Dis | year= 2015 | volume= 10 | issue= | pages= 66 | pmid=26025012 | doi=10.1186/s13023-015-0282-1 | pmc=4450481 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26025012 }} </ref> | |
| **Congenital hypopituitarism<ref name="pmid8157716">{{cite journal| author=Yagi H, Nagashima K, Miyake H, Tamai S, Onigata K, Yutani S et al.| title=Familial congenital hypopituitarism with central diabetes insipidus. | journal=J Clin Endocrinol Metab | year= 1994 | volume= 78 | issue= 4 | pages= 884-9 | pmid=8157716 | doi=10.1210/jcem.78.4.8157716 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8157716 }} </ref>
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| **Septo-optic dysplasia<ref name="pmid4191531">{{cite journal| author=Hoyt WF, Kaplan SL, Grumbach MM, Glaser JS| title=Septo-optic dysplasia and pituitary dwarfism. | journal=Lancet | year= 1970 | volume= 1 | issue= 7652 | pages= 893-4 | pmid=4191531 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4191531 }} </ref>
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| *Neurosurgery or trauma<ref name="pmid2492841">{{cite journal| author=Seckl J, Dunger D| title=Postoperative diabetes insipidus. | journal=BMJ | year= 1989 | volume= 298 | issue= 6665 | pages= 2-3 | pmid=2492841 | doi= | pmc=1835326 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2492841 }} </ref><ref name="pmid16235676">{{cite journal| author=Nemergut EC, Zuo Z, Jane JA, Laws ER| title=Predictors of diabetes insipidus after transsphenoidal surgery: a review of 881 patients. | journal=J Neurosurg | year= 2005 | volume= 103 | issue= 3 | pages= 448-54 | pmid=16235676 | doi=10.3171/jns.2005.103.3.0448 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16235676 }} </ref>
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| *Cancer<ref name="pmid6640507">{{cite journal| author=Kimmel DW, O'Neill BP| title=Systemic cancer presenting as diabetes insipidus. Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus. | journal=Cancer | year= 1983 | volume= 52 | issue= 12 | pages= 2355-8 | pmid=6640507 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6640507 }} </ref>
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| *Hypoxic encephalopathy
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| *Infiltrative disorders<ref name="pmid20434166">{{cite journal| author=Grois N, Fahrner B, Arceci RJ, Henter JI, McClain K, Lassmann H et al.| title=Central nervous system disease in Langerhans cell histiocytosis. | journal=J Pediatr | year= 2010 | volume= 156 | issue= 6 | pages= 873-81, 881.e1 | pmid=20434166 | doi=10.1016/j.jpeds.2010.03.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20434166 }} </ref><ref name="pmid2797079">{{cite journal| author=Dunger DB, Broadbent V, Yeoman E, Seckl JR, Lightman SL, Grant DB et al.| title=The frequency and natural history of diabetes insipidus in children with Langerhans-cell histiocytosis. | journal=N Engl J Med | year= 1989 | volume= 321 | issue= 17 | pages= 1157-62 | pmid=2797079 | doi=10.1056/NEJM198910263211704 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2797079 }} </ref>
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| **Langerhans cell histiocytosis (LCH)
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| **eosinophilic granuloma
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| *Post-supraventricular tachycardia<ref name="pmid6434116">{{cite journal| author=Canepa-Anson R, Williams M, Marshall J, Mitsuoka T, Lightman S, Sutton R| title=Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia. | journal=Br Med J (Clin Res Ed) | year= 1984 | volume= 289 | issue= 6449 | pages= 866-8 | pmid=6434116 | doi= | pmc=1443391 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6434116 }} </ref>
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| *Anorexia nervosa<ref name="pmid6835335">{{cite journal| author=Gold PW, Kaye W, Robertson GL, Ebert M| title=Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa. | journal=N Engl J Med | year= 1983 | volume= 308 | issue= 19 | pages= 1117-23 | pmid=6835335 | doi=10.1056/NEJM198305123081902 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6835335 }} </ref>
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| '''Nephrogenic DI''' | | ==='''Gestational Diabetes Insipidus'''=== |
| | *This type of [[diabetes insipidus]] occurs only during [[pregnancy]]. Gestational DI occurs when an [[enzyme]] made by the [[placenta]] destroys [[ADH]] produced in the mother. |
| | *Most cases of gestational DI can be successfully treated with [[desmopressin]].<ref name="pmid15153548" /> |
| | *In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and [[desmopressin]] should not be used.<ref name="pmid19384328">{{cite journal| author=Grünfeld JP, Rossier BC| title=Lithium nephrotoxicity revisited. | journal=Nat Rev Nephrol | year= 2009 | volume= 5 | issue= 5 | pages= 270-6 | pmid=19384328 | doi=10.1038/nrneph.2009.43 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19384328 }} </ref> |
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| The most common causes of ADH resistance severe enough to produce polyuria are hereditary nephrogenic DI in children, and chronic lithium ingestion and hypercalcemia in adults. Acquired causes are often partially reversible with cessation of the offending drug or correction of hypercalcemia. Other causes include;
| | ==='''Autoimmune Diabetes Insipidus'''=== |
| *Hereditary Nephrogenic Diabetes Insipidus<ref name="pmid10477148">{{cite journal| author=van Lieburg AF, Knoers NV, Monnens LA| title=Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 9 | pages= 1958-64 | pmid=10477148 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10477148 }} </ref>
| | *This type of [[diabetes insipidus]] is very rare. It results from an [[autoimmune]] cause.<ref name="pmid9329382" /> |
| **Vasopressin V2 receptor gene mutations<ref name="pmid15004257">{{cite journal| author=Sasaki S| title=Nephrogenic diabetes insipidus: update of genetic and clinical aspects. | journal=Nephrol Dial Transplant | year= 2004 | volume= 19 | issue= 6 | pages= 1351-3 | pmid=15004257 | doi=10.1093/ndt/gfh172 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15004257 }} </ref><ref name="pmid9329382">{{cite journal| author=Nomura Y, Onigata K, Nagashima T, Yutani S, Mochizuki H, Nagashima K et al.| title=Detection of skewed X-inactivation in two female carriers of vasopressin type 2 receptor gene mutation. | journal=J Clin Endocrinol Metab | year= 1997 | volume= 82 | issue= 10 | pages= 3434-7 | pmid=9329382 | doi=10.1210/jcem.82.10.4312 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9329382 }} </ref> | | *It is usually associated with other [[autoimmune]] diseases and typically affects women of childbearing age.<ref name="pmid9329382" /> |
| **Aquaporin-2 gene mutation<ref name="pmid15153548">{{cite journal| author=Devonald MA, Karet FE| title=Renal epithelial traffic jams and one-way streets. | journal=J Am Soc Nephrol | year= 2004 | volume= 15 | issue= 6 | pages= 1370-81 | pmid=15153548 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15153548 }} </ref>
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| *Lithium toxicity<ref name="pmid19384328">{{cite journal| author=Grünfeld JP, Rossier BC| title=Lithium nephrotoxicity revisited. | journal=Nat Rev Nephrol | year= 2009 | volume= 5 | issue= 5 | pages= 270-6 | pmid=19384328 | doi=10.1038/nrneph.2009.43 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19384328 }} </ref>
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| *Hypercalcemia<ref name="pmid3037155">{{cite journal| author=Berl T| title=The cAMP system in vasopressin-sensitive nephron segments of the vitamin D-treated rat. | journal=Kidney Int | year= 1987 | volume= 31 | issue= 5 | pages= 1065-71 | pmid=3037155 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3037155 }} </ref>
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| *Hypokalemia<ref name="pmid26674602">{{cite journal| author=Khositseth S, Uawithya P, Somparn P, Charngkaew K, Thippamom N, Hoffert JD et al.| title=Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus. | journal=Sci Rep | year= 2015 | volume= 5 | issue= | pages= 18311 | pmid=26674602 | doi=10.1038/srep18311 | pmc=4682130 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26674602 }} </ref>, Persistent severe hypokalemia (plasma potassium concentration usually below 3 meq/L) can impair urinary concentrating ability | |
| *Other — Nephrogenic DI has been described in a number of other clinical settings
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| **Renal disease
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| ***Sickle cell disease or trait
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| ***Autosomal dominant polycystic kidney disease
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| ***Medullary cystic kidney disease
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| ***Renal amyloidosis<ref name="pmid13807843">{{cite journal| author=CARONE FA, EPSTEIN FH| title=Nephrogenic diabetes insipidus caused by amyloid disease. Evidence in man of the role of the collecting ducts in concentrating urine. | journal=Am J Med | year= 1960 | volume= 29 | issue= | pages= 539-44 | pmid=13807843 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13807843 }} </ref>
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| ***Sjögren's syndrome<ref name="pmid14320699">{{cite journal| author=SHEARN MA, TU WH| title=NEPHROGENIC DIABETIC INSIPIDUS AND OTHER DEFECTS OF RENAL TUBULAR FUNCTION IN SJOERGREN'S SYNDROME. | journal=Am J Med | year= 1965 | volume= 39 | issue= | pages= 312-8 | pmid=14320699 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14320699 }} </ref>
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| **Drugs<ref name="pmid15806465">{{cite journal| author=Garofeanu CG, Weir M, Rosas-Arellano MP, Henson G, Garg AX, Clark WF| title=Causes of reversible nephrogenic diabetes insipidus: a systematic review. | journal=Am J Kidney Dis | year= 2005 | volume= 45 | issue= 4 | pages= 626-37 | pmid=15806465 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15806465 }} </ref>
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| ***Cidofovir
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| ***Foscarnet
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| ***Amphotericin B
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| ***Demeclocycline
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| ***Ifosfamide
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| ***Ofloxacin
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| ***Orlistat
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| ***Didanosine
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| **Pregnancy<ref name="pmid15863571">{{cite journal| author=Brewster UC, Hayslett JP| title=Diabetes insipidus in the third trimester of pregnancy. | journal=Obstet Gynecol | year= 2005 | volume= 105 | issue= 5 Pt 2 | pages= 1173-6 | pmid=15863571 | doi=10.1097/01.AOG.0000161811.02155.68 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15863571 }} </ref>
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| **Bardet-Biedl syndrome<ref name="pmid8270381">{{cite journal| author=Anadoliiska A, Roussinov D| title=Clinical aspects of renal involvement in Bardet-Biedl syndrome. | journal=Int Urol Nephrol | year= 1993 | volume= 25 | issue= 5 | pages= 509-14 | pmid=8270381 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8270381 }} </ref>
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| **Bartter syndrome<ref name="pmid11893344">{{cite journal| author=Peters M, Jeck N, Reinalter S, Leonhardt A, Tönshoff B, Klaus G Gü et al.| title=Clinical presentation of genetically defined patients with hypokalemic salt-losing tubulopathies. | journal=Am J Med | year= 2002 | volume= 112 | issue= 3 | pages= 183-90 | pmid=11893344 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11893344 }} </ref>
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| === Differentiating Diabetes insipidus based on the levels of ADH and the response of the body to the level of hyponatremia ===
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| *'''Disorders in which ADH levels are elevated'''<ref name="pmid25078421">{{cite journal| author=Danziger J, Zeidel ML| title=Osmotic homeostasis. | journal=Clin J Am Soc Nephrol | year= 2015 | volume= 10 | issue= 5 | pages= 852-62 | pmid=25078421 | doi=10.2215/CJN.10741013 | pmc=4422250 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25078421 }} </ref>
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| **Reduced effective arterial blood volume
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| ***True volume depletion
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| ***Heart failure
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| ***Cirrhosis
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| **Syndrome of inappropriate ADH secretion, including reset osmostat pattern
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| **Hormonal changes
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| ***Adrenal insufficiency
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| ***Hypothyroidism
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| ***Pregnancy
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| *'''Disorders in which ADH levels may be appropriately suppressed<ref name="pmid25551526">{{cite journal| author=Sterns RH| title=Disorders of plasma sodium--causes, consequences, and correction. | journal=N Engl J Med | year= 2015 | volume= 372 | issue= 1 | pages= 55-65 | pmid=25551526 | doi=10.1056/NEJMra1404489 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25551526 }} </ref>'''
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| **Advanced renal failure
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| **Primary polydipsia
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| **Beer drinker's potomania
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| **Diabetes mellitus
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| **Sickle cell disease
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| *'''Hyponatremia with normal or elevated plasma osmolality'''<ref name="pmid24722436">{{cite journal| author=Fenske WK, Christ-Crain M, Hörning A, Simet J, Szinnai G, Fassnacht M et al.| title=A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis. | journal=J Am Soc Nephrol | year= 2014 | volume= 25 | issue= 10 | pages= 2376-83 | pmid=24722436 | doi=10.1681/ASN.2013080895 | pmc=4178436 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24722436 }} </ref>
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| **High plasma osmolality (effective osmols)
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| ***Hyperglycemia
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| ***Mannitol
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| **High plasma osmolality (ineffective osmols)
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| ***Renal failure
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| ***Alcohol intoxication with an elevated serum alcohol concentration
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| **Normal plasma osmolality
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| ***Pseudohyponatremia (laboratory artifact)
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| ****High triglycerides
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| ****Cholestatic and obstructive jaundice (lipoprotein-X)
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| ****Multiple myeloma
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| ***Absorption of irrigant solutions
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| ****Glycine
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| ****Sorbitol
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| ****Mannitol
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|
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|
| ==References== | | ==References== |