Diabetes insipidus classification: Difference between revisions
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==Overview== | ==Overview== | ||
Diabetes insipidus can be classified into 3; [[central diabetes insipidus|central]], [[nephrogenic diabetes insipidus|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). | Diabetes insipidus can be classified into 3; [[central diabetes insipidus|central]], [[nephrogenic diabetes insipidus|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 age|gestational]] diabetes insipidus which occurs only in [[pregnancy]], [[autoimmune]] diabetes insipidus caused by an autoimmune reaction and thirst related diabetes insipidus. | ||
==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]]. Other causes include; | '''[[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]]. 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]]<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> | ||
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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. Other causes include;
- Hereditary nephrogenic diabetes insipidus[3]
- Vasopressin V2 receptor gene mutations[4][5]
- Aquaporin-2 gene mutation[6]
- Lithium toxicity[7]
- Hypercalcemia[8]
- Hypokalemia[9], 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
- Renal disease
- Drugs[12]
- Pregnancy[13]
- Bardet-Biedl syndrome[14]
- Bartter syndrome[15]
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.
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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Anadoliiska A, Roussinov D (1993). "Clinical aspects of renal involvement in Bardet-Biedl syndrome". Int Urol Nephrol. 25 (5): 509–14. PMID 8270381.
- ↑ 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.