Diabetes insipidus causes: Difference between revisions

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== Overview ==
== Overview ==
Diabetes insipidus is caused by a variety of factors. The causes for each subtype of diabetes insipidus is classically different. It is important to identify these underlying causes of the various forms in order to appropriately diagnose and treat each type.  
Diabetes insipidus is caused by a variety of factors. The causes for each sub type of diabetes insipidus is classically different. It is important to identify these underlying causes of the various forms in order to appropriately diagnose and treat each type.  


== Causes ==
== Causes ==


===Central DI===
===Central DI===
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>;
CDI is caused by the destruction or [[degeneration]] of [[neurons]] originating in the [[Supraoptic nucleus|supraoptic]] and [[Paraventricular nucleus|paraventricular nuclei]]. [[Central diabetes insipidus|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>;
*Familial and congenital disease
*[[Familial]] and [[Congenital disorder|congenital]] disease
**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>
**[[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>
**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>
**[[Wolfram syndrome]] also known as DIDMOAD ([[diabetes insipidus]], [[Diabetes mellitus|diabetes mellitus,]] [[Optic atrophy|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>
**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>
**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>
**[[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>
*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>
*[[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>
*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>
*[[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>
*Hypoxic encephalopathy
*[[Hypoxic encephalopathy]]
*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>
*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>
**Langerhans cell histiocytosis (LCH)
**[[Langerhans cell histiocytosis|Langerhans cell histiocytosis (LCH)]]
**eosinophilic granuloma
**[[eosinophilic granuloma]]
*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>
*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>
*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>
*[[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>


===Nephrogenic DI===
===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. Other causes include;
The most common causes of [[ADH]] resistance severe enough to produce [[polyuria]] are hereditary [[Nephrogenic diabetes insipidus|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;
*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>
*Hereditary [[Nephrogenic diabetes insipidus|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>
**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>
**[[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>
**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>
**[[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>
*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>
*[[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>
*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>
*[[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>
*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
*[[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
*Other — [[Nephrogenic diabetes insipidus|Nephrogenic DI]] has been described in a number of other clinical settings
**Renal disease  
**Renal disease  
***Sickle cell disease or trait
***[[Sickle-cell disease|Sickle cell disease]] or trait
***Autosomal dominant polycystic kidney disease
***[[Autosomal dominant polycystic kidney disease]]
***Medullary cystic kidney disease
***[[Medullary cystic kidney disease]]
***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>
***[[Amyloidosis|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>
***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>
***[[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>
**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>  
**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>  
***Cidofovir
***[[Cidofovir]]
***Foscarnet
***[[Foscarnet]]
***Amphotericin B
***[[Amphotericin B]]
***Demeclocycline
***[[Demeclocycline]]
***Ifosfamide
***[[Ifosfamide]]
***Ofloxacin
***[[Ofloxacin]]
***Orlistat
***[[Orlistat]]
***Didanosine
***[[Didanosine]]
**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>
**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>
**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>
**[[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>
**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>
**[[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>


===Psychogenic DI===
===Psychogenic DI===
Psychogenic DI also known as dipsogenic DI or primary polydispsia is characterized by a primary increase in water intake. This disorder is most often seen middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine which can lead to the sensation of a dry mouth. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosisis
Psychogenic DI also known as dipsogenic DI or primary [[polydipsia]] is characterized by a primary increase in water intake. This disorder is most often seen middle-aged women and in patients with psychiatric illnesses, including those taking a [[phenothiazine]] which can lead to the sensation of a dry mouth. Primary [[polydipsia]] can also be induced by [[hypothalamic]] lesions that directly affect the thirst center, as may occur with an infiltrative disease such as [[sarcoidosis]]


===Gestational DI===
===Gestational DI===
Gestational diabetes insipidus is an uncommon clinical disease whose prevalence is approximately 2-3 per 100,000 pregnancies. It results when an enzyme made by the placenta destroys ADH in the mother. The placenta is the system of blood vessels and other tissue that develops with the fetus. The placenta allows exchange of nutrients and waste products between mother and fetus.Most cases of gestational DI can be treated with desmopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used.
Gestational diabetes insipidus is an uncommon clinical disease whose prevalence is approximately 2-3 per 100,000 pregnancies. It results when an enzyme made by the [[placenta]] destroys [[ADH]] in the mother. The [[placenta]] is the system of blood vessels and other tissue that develops with the fetus. The placenta allows exchange of nutrients and waste products between mother and fetus.Most cases of gestational DI can be treated with [[desmopressin]]. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used.


===Causes by Organ System===
===Causes by Organ System===

Revision as of 13:12, 17 July 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Diabetes insipidus is caused by a variety of factors. The causes for each sub type of diabetes insipidus is classically different. It is important to identify these underlying causes of the various forms in order to appropriately diagnose and treat each type.

Causes

Central DI

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)[1][2]. Others include[2];

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. Other causes include;

Psychogenic DI

Psychogenic DI also known as dipsogenic DI or primary polydipsia is characterized by a primary increase in water intake. This disorder is most often seen middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine which can lead to the sensation of a dry mouth. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosis

Gestational DI

Gestational diabetes insipidus is an uncommon clinical disease whose prevalence is approximately 2-3 per 100,000 pregnancies. It results when an enzyme made by the placenta destroys ADH in the mother. The placenta is the system of blood vessels and other tissue that develops with the fetus. The placenta allows exchange of nutrients and waste products between mother and fetus.Most cases of gestational DI can be treated with desmopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used.

Causes by Organ System

Cardiovascular Hypovolemic shock
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect Amphotericin B, Demeclocycline, Lithium , Radiation - for CNS and nasopharyngeal malignancies , Pituitary radiation , Netilmicin , Kanamycin, Carbamazepine , Amikacin
Ear Nose Throat No underlying causes
Endocrine Ischemia of the pitutary gland , Sheehan syndrome , Pituitary tumour , Panhypopituitarism , lymphocytic hypophysitis , Familial hypopituitarism , congenital nephrogenic , Congenital hypopituitarism , Apoplexy , pituitary cysts
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic Inherited genetic kidney disorders , Genetic diseases - pit-1 mutation
Hematologic Sickle cell disease , Langerhans cell histiocytosis
Iatrogenic Neurosurgery , Pituitary surgery
Infectious Disease Tuberculous meningitis , Meningoencephalitis , Infections
Musculoskeletal / Ortho No underlying causes
Neurologic Dipsogenic diabetes insipidus , Ischemic encephalopathy , Subarachnoid hemorrhage , Mass lesions hypothalamus , Ischemic stroke , Intracranial space-occupying lesion , Intracranial bleeding , Hypoxic encephalopathy , Hypothalamic radiation , Brain aneurysm
Nutritional / Metabolic Hypercalcemia , hemochromatosis , Anorexia nervosa
Obstetric/Gynecologic Gestational diabetes insipidus
Oncologic Pituitary Cancer , pituitary adenomas , malignant tumors infilterating hypothalamus from lung and breast , Histiocytosis , Craniopharyngioma
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal / Electrolyte Polycystic kidney disease, Renal failure , Interstitial nephritis , Hypokalaemia , Hypercalcaemia
Rheum / Immune / Allergy Sarcoidosis , Autoimmune Hypophysitis , Autoimmune Diabetes Insipidus
Sexual No underlying causes
Trauma Head injury , Trauma - fracture of skull base
Urologic Partial blockage of the ureters
Dental No underlying causes
Miscellaneous Dehydration , Wolfram syndrome , Sicca syndrome , Septo-optic dysplasia , Infiltrative lesions , Idiopathic , Hand-Schuller-Christian Syndrome , Familial CDI , Erdheim-Chester disease , DIDMOAD syndrome , Anophthalmia -- hypyothalamo-pituitary insufficiency , Anophthalmia -- hypothalamo-pituitary insufficiency , Amyloidosis

Causes in Alphabetical Order


References

  1. ↑ 1.0 1.1 Kimmel DW, O'Neill BP (1983). "Systemic cancer presenting as diabetes insipidus. Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus". Cancer. 52 (12): 2355–8. PMID 6640507.
  2. ↑ 2.0 2.1 Maghnie M, Cosi G, Genovese E, Manca-Bitti ML, Cohen A, Zecca S; et al. (2000). "Central diabetes insipidus in children and young adults". N Engl J Med. 343 (14): 998–1007. doi:10.1056/NEJM200010053431403. PMID 11018166.
  3. ↑ Burbach JP, Luckman SM, Murphy D, Gainer H (2001). "Gene regulation in the magnocellular hypothalamo-neurohypophysial system". Physiol Rev. 81 (3): 1197–267. PMID 11427695.
  4. ↑ Bischoff AN, Reiersen AM, Buttlaire A, Al-Lozi A, Doty T, Marshall BA; et al. (2015). "Selective cognitive and psychiatric manifestations in Wolfram Syndrome". Orphanet J Rare Dis. 10: 66. doi:10.1186/s13023-015-0282-1. PMC 4450481. PMID 26025012.
  5. ↑ Yagi H, Nagashima K, Miyake H, Tamai S, Onigata K, Yutani S; et al. (1994). "Familial congenital hypopituitarism with central diabetes insipidus". J Clin Endocrinol Metab. 78 (4): 884–9. doi:10.1210/jcem.78.4.8157716. PMID 8157716.
  6. ↑ Hoyt WF, Kaplan SL, Grumbach MM, Glaser JS (1970). "Septo-optic dysplasia and pituitary dwarfism". Lancet. 1 (7652): 893–4. PMID 4191531.
  7. ↑ Seckl J, Dunger D (1989). "Postoperative diabetes insipidus". BMJ. 298 (6665): 2–3. PMC 1835326. PMID 2492841.
  8. ↑ Nemergut EC, Zuo Z, Jane JA, Laws ER (2005). "Predictors of diabetes insipidus after transsphenoidal surgery: a review of 881 patients". J Neurosurg. 103 (3): 448–54. doi:10.3171/jns.2005.103.3.0448. PMID 16235676.
  9. ↑ Grois N, Fahrner B, Arceci RJ, Henter JI, McClain K, Lassmann H; et al. (2010). "Central nervous system disease in Langerhans cell histiocytosis". J Pediatr. 156 (6): 873–81, 881.e1. doi:10.1016/j.jpeds.2010.03.001. PMID 20434166.
  10. ↑ Dunger DB, Broadbent V, Yeoman E, Seckl JR, Lightman SL, Grant DB; et al. (1989). "The frequency and natural history of diabetes insipidus in children with Langerhans-cell histiocytosis". N Engl J Med. 321 (17): 1157–62. doi:10.1056/NEJM198910263211704. PMID 2797079.
  11. ↑ Canepa-Anson R, Williams M, Marshall J, Mitsuoka T, Lightman S, Sutton R (1984). "Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia". Br Med J (Clin Res Ed). 289 (6449): 866–8. PMC 1443391. PMID 6434116.
  12. ↑ Gold PW, Kaye W, Robertson GL, Ebert M (1983). "Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa". N Engl J Med. 308 (19): 1117–23. doi:10.1056/NEJM198305123081902. PMID 6835335.
  13. ↑ van Lieburg AF, Knoers NV, Monnens LA (1999). "Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus". J Am Soc Nephrol. 10 (9): 1958–64. PMID 10477148.
  14. ↑ Sasaki S (2004). "Nephrogenic diabetes insipidus: update of genetic and clinical aspects". Nephrol Dial Transplant. 19 (6): 1351–3. doi:10.1093/ndt/gfh172. PMID 15004257.
  15. ↑ Nomura Y, Onigata K, Nagashima T, Yutani S, Mochizuki H, Nagashima K; et al. (1997). "Detection of skewed X-inactivation in two female carriers of vasopressin type 2 receptor gene mutation". J Clin Endocrinol Metab. 82 (10): 3434–7. doi:10.1210/jcem.82.10.4312. PMID 9329382.
  16. ↑ Devonald MA, Karet FE (2004). "Renal epithelial traffic jams and one-way streets". J Am Soc Nephrol. 15 (6): 1370–81. PMID 15153548.
  17. ↑ Grünfeld JP, Rossier BC (2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol. 5 (5): 270–6. doi:10.1038/nrneph.2009.43. PMID 19384328.
  18. ↑ Berl T (1987). "The cAMP system in vasopressin-sensitive nephron segments of the vitamin D-treated rat". Kidney Int. 31 (5): 1065–71. PMID 3037155.
  19. ↑ Khositseth S, Uawithya P, Somparn P, Charngkaew K, Thippamom N, Hoffert JD; et al. (2015). "Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus". Sci Rep. 5: 18311. doi:10.1038/srep18311. PMC 4682130. PMID 26674602.
  20. ↑ CARONE FA, EPSTEIN FH (1960). "Nephrogenic diabetes insipidus caused by amyloid disease. Evidence in man of the role of the collecting ducts in concentrating urine". Am J Med. 29: 539–44. PMID 13807843.
  21. ↑ SHEARN MA, TU WH (1965). "NEPHROGENIC DIABETIC INSIPIDUS AND OTHER DEFECTS OF RENAL TUBULAR FUNCTION IN SJOERGREN'S SYNDROME". Am J Med. 39: 312–8. PMID 14320699.
  22. ↑ Garofeanu CG, Weir M, Rosas-Arellano MP, Henson G, Garg AX, Clark WF (2005). "Causes of reversible nephrogenic diabetes insipidus: a systematic review". Am J Kidney Dis. 45 (4): 626–37. PMID 15806465.
  23. ↑ Brewster UC, Hayslett JP (2005). "Diabetes insipidus in the third trimester of pregnancy". Obstet Gynecol. 105 (5 Pt 2): 1173–6. doi:10.1097/01.AOG.0000161811.02155.68. PMID 15863571.
  24. ↑ Anadoliiska A, Roussinov D (1993). "Clinical aspects of renal involvement in Bardet-Biedl syndrome". Int Urol Nephrol. 25 (5): 509–14. PMID 8270381.
  25. ↑ Peters M, Jeck N, Reinalter S, Leonhardt A, Tönshoff B, Klaus G Gü; et al. (2002). "Clinical presentation of genetically defined patients with hypokalemic salt-losing tubulopathies". Am J Med. 112 (3): 183–90. PMID 11893344.


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