Diabetes insipidus classification: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(28 intermediate revisions by 4 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Diabetes insipidus}}
{{Diabetes insipidus}}
{{CMG}}
{{CMG}}; {{AE}} {{DAMI}}
==Overview==
==Overview==
== Classification ==
[[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.
There are several forms of DI:
 
* ''Central'' diabetes insipidus is due to damage to the hypothalamus or pituitary due to a [[tumor]], [[cerebrovascular accident|stroke]], [[neurosurgery]] or some rather rare causes (which include [[hemochromatosis]], [[sarcoidosis]], [[histiocytosis]], diseases that can form masses in the vicinity like a [[tuberculoma]] or [[syphilis]] and some [[genetic disorder]]s). If the hypothalamus is damaged, the feeling of thirst may be completely absent.
==Classification==
* ''Nephrogenic'' diabetes insipidus is due to the inability of the kidney to respond normally to ADH. There are hereditary causes (90% are due to mutations of the ADH V2 receptor, and 10% mutations of the [[aquaporin#AQP2|aquaporin 2]] water channel), but these are rare (incidence is around 4 per million live births). Most are male, because V2 receptor mutations are x-linked recessive defects. More common are acquired forms of NDI, which occur as a side-effect to some [[medication]]s (such as [[lithium citrate]] and [[amphotericin B]]), as well as in [[polycystic kidney disease]] (PKD) and [[sickle-cell disease]], and electrolyte disturbances such as hypokalaemia and hypercalcaemia. In some cases, no cause is found.
==='''[[Central diabetes insipidus|Central DI]]'''===
* ''Dipsogenic'' DI is due to a defect or damage to the thirst mechanism, which is located in the hypothalamus. This defect results in an abnormal increase in thirst and fluid intake that suppresses ADH secretion and increases urine output. Desmopressin is ineffective, and can lead to fluid overload as the thirst remains.
*[[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]].  
* ''Gestational'' DI only occurs during [[pregnancy]]. While all pregnant women produce ''vasopressinase'' in the [[placenta]], which breaks down ADH, this can assume extreme forms in GDI. 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.
*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]]'''===
*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>
 
==='''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.<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>
*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>
 
==='''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>
 
==='''Autoimmune Diabetes Insipidus'''===
*This type of [[diabetes insipidus]] is very rare. It results from an [[autoimmune]] cause.<ref name="pmid9329382" />
*It is usually associated with other [[autoimmune]] diseases and typically affects women of childbearing age.<ref name="pmid9329382" />
 
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Latest revision as of 19:36, 26 October 2017

Diabetes insipidus Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Diabetes insipidus from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-Ray

CT scan

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Diabetes insipidus classification On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Diabetes insipidus classification

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Diabetes insipidus classification

CDC on Diabetes insipidus classification

Diabetes insipidus classification in the news

Blogs on Diabetes insipidus classification

Directions to Hospitals Treating Diabetes insipidus

Risk calculators and risk factors for Diabetes insipidus classification

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

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]

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.[6]
  • 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.[7]

Gestational Diabetes Insipidus

Autoimmune Diabetes Insipidus

References

  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. 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. 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.
  4. 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.
  5. 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.
  6. 6.0 6.1 Devonald MA, Karet FE (2004). "Renal epithelial traffic jams and one-way streets". J Am Soc Nephrol. 15 (6): 1370–81. PMID 15153548.
  7. 7.0 7.1 7.2 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.
  8. Grünfeld JP, Rossier BC (2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol. 5 (5): 270–6. doi:10.1038/nrneph.2009.43. PMID 19384328.


Template:WikiDoc Sources