Diabetes insipidus classification

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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]


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.


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


  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.

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