Diabetes insipidus classification

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

Overview

Diabetes Insipidus can be classified into 4; Central, Nephrogenic, Psychogenic and Gestational diabetes insipidus. It can also be classified 2; Disorders in which ADH levels are elevated and Disorders in which ADH levels may be appropriately suppressed[1] based on the levels of ADH present in the body and the levels of hypo- or hypernatremia.

Classification

Classification into central vs nephrogenic DI

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)[2][3]. Others include[3];

  • Familial and congenital disease
    • Familial CDI[4]
    • Wolfram syndrome also known as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness)[5]
    • Congenital hypopituitarism[6]
    • Septo-optic dysplasia[7]
  • Neurosurgery or trauma[8][9]
  • Cancer[2]
  • Hypoxic encephalopathy
  • Infiltrative disorders[10][11]
    • Langerhans cell histiocytosis (LCH)
    • eosinophilic granuloma
  • Post-supraventricular tachycardia[12]
  • Anorexia nervosa[13]

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[14]
    • Vasopressin V2 receptor gene mutations[15][16]
    • Aquaporin-2 gene mutation[17]
  • Lithium toxicity[18]
  • Hypercalcemia[19]
  • Hypokalemia[20], 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[21]
      • Sjögren's syndrome[22]
    • Drugs[23]
      • Cidofovir
      • Foscarnet
      • Amphotericin B
      • Demeclocycline
      • Ifosfamide
      • Ofloxacin
      • Orlistat
      • Didanosine
    • Pregnancy[24]
    • Bardet-Biedl syndrome[25]
    • Bartter syndrome[26]


Differentiating Diabetes insipidus based on the levels of ADH and the response of the body to the level of hyponatremia

  • Disorders in which ADH levels are elevated[27]
    • Reduced effective arterial blood volume
      • True volume depletion
      • Heart failure
      • Cirrhosis
    • Syndrome of inappropriate ADH secretion, including reset osmostat pattern
    • Hormonal changes
      • Adrenal insufficiency
      • Hypothyroidism
      • Pregnancy
  • Disorders in which ADH levels may be appropriately suppressed[1]
    • Advanced renal failure
    • Primary polydipsia
    • Beer drinker's potomania
    • Diabetes mellitus
    • Sickle cell disease
  • Hyponatremia with normal or elevated plasma osmolality[28]
    • High plasma osmolality (effective osmols)
      • Hyperglycemia
      • Mannitol
    • High plasma osmolality (ineffective osmols)
      • Renal failure
      • Alcohol intoxication with an elevated serum alcohol concentration
    • Normal plasma osmolality
      • Pseudohyponatremia (laboratory artifact)
        • High triglycerides
        • Cholestatic and obstructive jaundice (lipoprotein-X)
        • Multiple myeloma
      • Absorption of irrigant solutions
        • Glycine
        • Sorbitol
        • Mannitol

References

  1. ↑ 1.0 1.1 Sterns RH (2015). "Disorders of plasma sodium--causes, consequences, and correction". N Engl J Med. 372 (1): 55–65. doi:10.1056/NEJMra1404489. PMID 25551526.
  2. ↑ 2.0 2.1 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.
  3. ↑ 3.0 3.1 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ Hoyt WF, Kaplan SL, Grumbach MM, Glaser JS (1970). "Septo-optic dysplasia and pituitary dwarfism". Lancet. 1 (7652): 893–4. PMID 4191531.
  8. ↑ Seckl J, Dunger D (1989). "Postoperative diabetes insipidus". BMJ. 298 (6665): 2–3. PMC 1835326. PMID 2492841.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ Devonald MA, Karet FE (2004). "Renal epithelial traffic jams and one-way streets". J Am Soc Nephrol. 15 (6): 1370–81. PMID 15153548.
  18. ↑ Grünfeld JP, Rossier BC (2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol. 5 (5): 270–6. doi:10.1038/nrneph.2009.43. PMID 19384328.
  19. ↑ 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.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ Anadoliiska A, Roussinov D (1993). "Clinical aspects of renal involvement in Bardet-Biedl syndrome". Int Urol Nephrol. 25 (5): 509–14. PMID 8270381.
  26. ↑ 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.
  27. ↑ Danziger J, Zeidel ML (2015). "Osmotic homeostasis". Clin J Am Soc Nephrol. 10 (5): 852–62. doi:10.2215/CJN.10741013. PMC 4422250. PMID 25078421.
  28. ↑ Fenske WK, Christ-Crain M, Hörning A, Simet J, Szinnai G, Fassnacht M; et al. (2014). "A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis". J Am Soc Nephrol. 25 (10): 2376–83. doi:10.1681/ASN.2013080895. PMC 4178436. PMID 24722436.


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