Diabetes insipidus classification: Difference between revisions
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==Classification== | ==Classification== | ||
'''[[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]]), 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>. | '''[[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]]), 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>. | ||
'''[[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]]. | '''[[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''': is characterized primarily by an excess of water intake. This disorder is most often seen 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 are [[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. | '''Psychogenic Diabetes insipidus''': is characterized primarily by an excess of water intake. This disorder is most often seen 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 are [[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''': This type of diabetes insipidus occurs only in pregnancy. Gestational DI occurs when an enzyme made by the placenta destroys ADH produced in the mother. 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. | |||
'''Autoimmune diabetes insipidus''': This type of diabetes insipidus is very rare. It is due to an autoimmune cause. It is usually associated with other autoimmune diseases and typically affects women of child-bearing age. | |||
==References== | ==References== | ||
Revision as of 14:21, 1 August 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Diabetes insipidus can be classified into 3; central, nephrogenic, and psychogenic diabetes insipidus which is due to a defect in water balance leading to the excretion of large volumes of dilute urine (urine osmolality usually below 250 mosmol/kg). Some rarer types of diabetes insipidus include gestational diabetes insipidus which occurs only in pregnancy, autoimmune diabetes insipidus caused by an autoimmune reaction and thirst related diabetes insipidus.
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), accounting for the vast majority of cases, are idiopathic diabetes insipidus (DI)[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: is characterized primarily by an excess of water intake. This disorder is most often seen 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 are 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 in pregnancy. Gestational DI occurs when an enzyme made by the placenta destroys ADH produced in the mother. 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.
Autoimmune diabetes insipidus: This type of diabetes insipidus is very rare. It is due to an autoimmune cause. It is usually associated with other autoimmune diseases and typically affects women of child-bearing 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.