Diabetes insipidus classification: Difference between revisions

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== Classification ==
== Classification ==
There are several forms of DI:
===Central 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.
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>;
* ''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.
*Familial and congenital disease
* ''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.
**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>
* ''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.
**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>
**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>
*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>
*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>
**Langerhans cell histiocytosis (LCH)
**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>
*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===
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>
**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>
*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>
*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
**Renal disease
***Sickle cell disease or trait
***Autosomal dominant polycystic 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>
***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>
***Cidofovir
***Foscarnet
***Amphotericin B
***Demeclocycline
***Ifosfamide
***Ofloxacin
***Orlistat
***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>
**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>
 
===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
 
===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.
 
==References==
==References==
{{reflist|2}}
{{reflist|2}}

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

Overview

Diabetes Insipidus can be classified into central and nephrogenic diabetes insipidus based on the response of the body to administration of desmopressin (DDAVP). Diabetes insipidus can also be classified into 5 based on the complaint of hypotonic polyuria, polydipsia and nocturia. The 4 types include; Central DI, Nephrogenic DI, Psychogenic DI, Gestational DI.

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]. Others include[2];

  • Familial and congenital disease
    • Familial CDI[3]
    • Wolfram syndrome also known as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness)[4]
    • Congenital hypopituitarism[5]
    • Septo-optic dysplasia[6]
  • Neurosurgery or trauma[7][8]
  • Cancer[1]
  • Hypoxic encephalopathy
  • Infiltrative disorders[9][10]
    • Langerhans cell histiocytosis (LCH)
    • eosinophilic granuloma
  • Post-supraventricular tachycardia[11]
  • Anorexia nervosa[12]

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[13]
    • Vasopressin V2 receptor gene mutations[14][15]
    • Aquaporin-2 gene mutation[16]
  • Lithium toxicity[17]
  • Hypercalcemia[18]
  • Hypokalemia[19], 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
      • Sickle cell disease or trait
      • Autosomal dominant polycystic kidney disease
      • Medullary cystic kidney disease
      • Renal amyloidosis[20]
      • Sjögren's syndrome[21]
    • Drugs[22]
      • Cidofovir
      • Foscarnet
      • Amphotericin B
      • Demeclocycline
      • Ifosfamide
      • Ofloxacin
      • Orlistat
      • Didanosine
    • Pregnancy[23]
    • Bardet-Biedl syndrome[24]
    • Bartter syndrome[25]

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

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.

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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