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==Classification== | ==Classification== | ||
'''[[Central diabetes insipidus|Central 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]]. [[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]]) 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> | |||
'''[[Nephrogenic diabetes insipidus|Nephrogenic 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="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><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><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><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> | |||
'''Psychogenic Diabetes Insipidus''' | ==='''Psychogenic Diabetes Insipidus'''=== | ||
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. 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. | |||
'''Gestational Diabetes Insipidus''' | ==='''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]]. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and [[desmopressin]] should not be used. | |||
'''Autoimmune Diabetes Insipidus''' | ==='''Autoimmune Diabetes Insipidus'''=== | ||
This type of [[diabetes insipidus]] is very rare. It results from an [[autoimmune]] cause. It is usually associated with other [[autoimmune]] diseases and typically affects women of childbearing age. | |||
==References== | ==References== | ||
Revision as of 20:40, 11 October 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]
Overview
Diabetes insipidus can be classified into three types: central, nephrogenic, and psychogenic diabetes insipidus. Some rare forms of the disease include gestational diabetes insipidus, which occurs only in pregnancy, and autoimmune diabetes insipidus, which is caused by an autoimmune reaction.
Classification
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) is idiopathic diabetes insipidus (DI), which accounts for the vast majority of cases of CDI.[1][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.[3][4][5][6][7][8]
Psychogenic Diabetes Insipidus
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 illnesses, including those taking a phenothiazine, which can lead to the sensation of a dry mouth. Other identifiable causes of psychogenic diabetes insipidus include sarcoidosis and lesions to the hypothalamic pituitary axis, which may disrupt the thirst center, thereby increasing the sensation of thirst and water consumption.
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. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used.
Autoimmune Diabetes Insipidus
This type of diabetes insipidus is very rare. It results from an autoimmune cause. It is usually associated with other autoimmune diseases and typically affects women of childbearing age.
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Devonald MA, Karet FE (2004). "Renal epithelial traffic jams and one-way streets". J Am Soc Nephrol. 15 (6): 1370–81. PMID 15153548.
- ↑ Grünfeld JP, Rossier BC (2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol. 5 (5): 270–6. doi:10.1038/nrneph.2009.43. PMID 19384328.
- ↑ 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.