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

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 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) Increased AVP metabolism     Pregnancy















  • 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
  • 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

References

  1. 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.
  2. 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.
  3. 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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