Differentiating Diabetes insipidus from other diseases: Difference between revisions

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Revision as of 13:28, 12 July 2017

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

Overview

Diabetes insipidus must be differentiated from other diseases that cause polyuria which is defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children, increased frequency or nocturia and polydipsia. It is important to know that levels of hypo or hypernatremia is not sufficient to describe the underlying cause of diabetes insipidus.

Differentiating Diabetes insipidus from other Diseases

Differentiating diabetes insipidus based on the type of diabetes insipidus caused

Central diabetes insipidus
- Acquired
  - Trauma (surgery, deceleration injury)
  - Vascular (cerebral hemorrhage, infarctionanterior communicating artery aneurysm or ligation, intrahypothalamic hemorrhage)
  - Neoplastic (craniopharyngioma, meningioma, germinoma, pituitary tumor or metastases)
  - Granulomatous (histiocytosis, sarcoidosis)
  - Infectious (meningitis, encephalitis)
  - Inflammatory/autoimmune (lymphocytic infundibuloneurohypophysitis)
  - Drug/toxin-induced (ethanol, diphenylhydantoin, snake venom)
  - Other disorders (hydrocephalus, ventricular/suprasellar cyst, trauma, degenerative diseases)
  - Idiopathic
- Congenital
  - Congenital malformations
    - Autosomal dominant: AVP-neurophysin gene mutations
    - Autosomal recessive ^[1]^[2]: Wolfram Syndrome (DIDMOAD) ^[3]
    - X-linked recessive
  - Idiopathic
Nephrogenic diabetes insipidus
- Acquired
  - Drug-induced (demeclocycline, lithium, cisplatin, methoxyflurane, etc.)
  - Hypercalcemia, hypokalemia
  - Infiltrating lesions (sarcoidosis, amyloidosis, multiple myeloma, Sjoergen's disease)
  - Vascular (sickle cell disease)
- Congenital
  - X-linked recessive (OMIM 304800): AVP V2 receptor gene mutations
  - Autosomal recessive: AQP2 water channel gene mutations
Primary polydipsia
- Psychogenic
- Dipsogenic (downward resetting of thirst threshold)
Pregnancy
Diabetes meliitus
Sickle cell disease

References

↑ Willcutts MD, Felner E, White PC (1999). "Autosomal recessive familial neurohypophyseal diabetes insipidus with continued secretion of mutant weakly active vasopressin". Hum Mol Genet. 8 (7): 1303–7. PMID 10369876.
↑ Abu Libdeh A, Levy-Khademi F, Abdulhadi-Atwan M, Bosin E, Korner M, White PC; et al. (2010). "Autosomal recessive familial neurohypophyseal diabetes insipidus: onset in early infancy". Eur J Endocrinol. 162 (2): 221–6. doi:10.1530/EJE-09-0772. PMID 19897608.
↑ Barrett TG, Bundey SE (1997). "Wolfram (DIDMOAD) syndrome". J Med Genet. 34 (10): 838–41. PMC 1051091. PMID 9350817.

Template:WH Template:WS

[pmid10369876-1] Willcutts MD, Felner E, White PC (1999). "Autosomal recessive familial neurohypophyseal diabetes insipidus with continued secretion of mutant weakly active vasopressin". Hum Mol Genet. 8 (7): 1303–7. PMID 10369876.

[pmid19897608-2] Abu Libdeh A, Levy-Khademi F, Abdulhadi-Atwan M, Bosin E, Korner M, White PC; et al. (2010). "Autosomal recessive familial neurohypophyseal diabetes insipidus: onset in early infancy". Eur J Endocrinol. 162 (2): 221–6. doi:10.1530/EJE-09-0772. PMID 19897608.

[pmid9350817-3] Barrett TG, Bundey SE (1997). "Wolfram (DIDMOAD) syndrome". J Med Genet. 34 (10): 838–41. PMC 1051091. PMID 9350817.

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[2]

[3]

@@ Line 40: / Line 40: @@
 *'''Diabetes meliitus'''
 *'''Sickle cell disease'''
-=== 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'''<ref name="pmid25078421">{{cite journal| author=Danziger J, Zeidel ML| title=Osmotic homeostasis. | journal=Clin J Am Soc Nephrol | year= 2015 | volume= 10 | issue= 5 | pages= 852-62 | pmid=25078421 | doi=10.2215/CJN.10741013 | pmc=4422250 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25078421  }} </ref>
-**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<ref name="pmid25551526">{{cite journal| author=Sterns RH| title=Disorders of plasma sodium--causes, consequences, and correction. | journal=N Engl J Med | year= 2015 | volume= 372 | issue= 1 | pages= 55-65 | pmid=25551526 | doi=10.1056/NEJMra1404489 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25551526  }} </ref>'''
-**Advanced renal failure
-**Primary polydipsia
-**Beer drinker's potomania
-**Diabetes mellitus
-**Sickle cell disease
-*'''Hyponatremia with normal or elevated plasma osmolality'''<ref name="pmid24722436">{{cite journal| author=Fenske WK, Christ-Crain M, Hörning A, Simet J, Szinnai G, Fassnacht M et al.| title=A copeptin-based classification of the osmoregulatory defects in the syndrome of inappropriate antidiuresis. | journal=J Am Soc Nephrol | year= 2014 | volume= 25 | issue= 10 | pages= 2376-83 | pmid=24722436 | doi=10.1681/ASN.2013080895 | pmc=4178436 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24722436  }} </ref>
-**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 {| class="wikitable" ! ! ! ! |- | | | | |- | | | | |- | | | | |}
 ==References==