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. 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, infarction, anterior communicating artery aneurysm or ligation, intra-hypothalamic 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
- Congenital malformations
- Acquired
- Nephrogenic diabetes insipidus
- Acquired
- Drug-induced (demeclocycline, lithium, cisplatin, methoxyflurane, etc.)
- Hypercalcemia, hypokalemia
- Infiltrating lesions (sarcoidosis, amyloidosis, multiple myeloma, Sjogren'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)
- Gestational Diabetes insipidus
- Diabetes meliitus
| Type of DI | Subclass | Disease | Defining signs and symptoms | Lab/Imaging findings |
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| Central | Acquired | Histiocytosis |
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| Craniopharyngioma |
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| Sarcoidosis |
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| Congenital | Hydrocephalus |
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Dilated ventricles on CT and MRI | |
| Wolfram Syndrome (DIDMOAD) |
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| Nephrogenic | Acquired | Drug-induced (demeclocycline, lithium) |
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| Hypercalcemia |
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| Hypokalemia |
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| Multiple myeloma |
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| Sickle cell disease |
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| Primary polydipsia | Psychogenic |
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| Pregnancy | Gestational diabetes insipidus |
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| Diabetes mellitus |
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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.
- ↑ Ghosh KN, Bhattacharya A (1992). "Gonotrophic nature of Phlebotomus argentipes (Diptera: Psychodidae) in the laboratory". Rev Inst Med Trop Sao Paulo. 34 (2): 181–2. PMID 1340034.