Differentiating Diabetes insipidus from other diseases
|
Diabetes insipidus Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Differentiating Diabetes insipidus from other diseases On the Web |
|
American Roentgen Ray Society Images of Differentiating Diabetes insipidus from other diseases |
|
FDA on Differentiating Diabetes insipidus from other diseases |
|
CDC on Differentiating Diabetes insipidus from other diseases |
|
Differentiating Diabetes insipidus from other diseases in the news |
|
Blogs on Differentiating Diabetes insipidus from other diseases |
|
Risk calculators and risk factors for Differentiating Diabetes insipidus from other diseases |
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 diabetes insipidus can be differentaited in several ways, 2 of which are described below. 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 (21, 22): Wolfram Syndrome (DIDMOAD) (23)
- X-linked recessive (24)
- Idiopathic
- Congenital malformations
- Acquired
- 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
- Acquired
- Primary polydipsia
- Psychogenic
- Dipsogenic (downward resetting of thirst threshold)
- Increased AVP metabolism
- Pregnancy
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[1]
- 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
- Reduced effective arterial blood volume
- Disorders in which ADH levels may be appropriately suppressed[2]
- Advanced renal failure
- Primary polydipsia
- Beer drinker's potomania
- Hyponatremia with normal or elevated plasma osmolality[3]
- 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
- Pseudohyponatremia (laboratory artifact)
- High plasma osmolality (effective osmols)
References
- ↑ 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.
- ↑ 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.
- ↑ 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.