Differentiating Diabetes insipidus from other diseases
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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.
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.