Nephrogenic diabetes insipidus causes
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Acquired
Nephrogenic DI (NDI) is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis,[1] polycystic kidney disease,[2] electrolyte imbalance,[3][4] or some other kidney defect.[1]
The major causes of acquired NDI that produce clinical symptoms (e.g. polyuria) in the adult are lithium toxicity and hypercalcemia. Chronic lithium ingestion - appears to affect the tubules by entering the collecting tubule cells through sodium channels, accumulating and interfering with the normal response to ADH (ADH Resistance) in a mechanism that is not yet fully understood. Hypercalcemia causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the calcium-sensing receptor (CaSR).
- Osmotic
Other causes of acquired NDI include: hypokalemia, post-obstructive polyuria, sickle cell disease/trait, amyloidosis, Sjogren syndrome, renal cystic disease, Bartter syndrome and various drugs (Amphotericin B, Orlistat, Ifosfomide, Ofloxacin, Cidofovir, Vaptanes).
In addition to kidney and systemic disorders, nephrogenic DI can present itself as a side-effect to some medications. The most common and well known of these drugs is lithium,[5] although there are numerous other medications that cause this effect with lesser frequency.[1]
Hereditary
This form of DI can also be hereditary:
| Type | OMIM | Gene | Locus |
|---|---|---|---|
| NDI1 | 304800 | AVPR2 | Usually, the hereditary form of nephrogenic DI is the result of an X-linked genetic defect which causes the vasopressin receptor (also called the V2 receptor) in the kidney to not function correctly.[1][6] |
| NDI2 | 125800 | AQP2 | In more rare cases, a mutation in the "aquaporin 2" gene impede the normal functionality of the kidney water channel, which results in the kidney being unable to absorb water. This mutation is often inherited in an autosomal recessive manner although dominant mutations are reported from time to time [1][7] |
Causes
Life Threatening Causes
Common Causes
| Cardiovascular | No underlying causes |
| Chemical/Poisoning | No underlying causes |
| Dental | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | Streptozocin |
| Ear Nose Throat | No underlying causes |
| Endocrine | No underlying causes |
| Environmental | No underlying causes |
| Gastroenterologic | No underlying causes |
| Genetic | No underlying causes |
| Hematologic | No underlying causes |
| Iatrogenic | No underlying causes |
| Infectious Disease | No underlying causes |
| Musculoskeletal/Orthopedic | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional/Metabolic | No underlying causes |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | No underlying causes |
| Ophthalmologic | No underlying causes |
| Overdose/Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | No underlying causes |
| Renal/Electrolyte | No underlying causes |
| Rheumatology/Immunology/Allergy | No underlying causes |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Miscellaneous | No underlying causes |
Causes in Alphabetical Order
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References
- ↑ 1.0 1.1 1.2 1.3 1.4 Template:Cite document http://www.diabetesinsipidus.org/4_types_nephrogenic_di.htm
- ↑ http://kidney.niddk.nih.gov/kudiseases/pubs/insipidus/index.htm
- ↑ Marples D, Frøkiaer J, Dørup J, Knepper MA, Nielsen S (April 1996). "Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex". J. Clin. Invest. 97 (8): 1960–8. doi:10.1172/JCI118628. PMC 507266. PMID 8621781.
- ↑ Carney S, Rayson B, Morgan T (October 1976). "A study in vitro of the concentrating defect associated with hypokalaemia and hypercalcaemia". Pflugers Arch. 366 (1): 11–7. doi:10.1007/BF02486556. PMID 185584.
- ↑ Christensen S, Kusano E, Yusufi AN, Murayama N, Dousa TP (June 1985). "Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats". J. Clin. Invest. 75 (6): 1869–79. doi:10.1172/JCI111901. PMC 425543. PMID 2989335.
- ↑ Online Mendelian Inheritance in Man (OMIM) DIABETES INSIPIDUS, NEPHROGENIC, X-LINKED -304800
- ↑ Online Mendelian Inheritance in Man (OMIM) DIABETES INSIPIDUS, NEPHROGENIC, AUTOSOMAL -125800