Diabetes insipidus risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
The risk factors in the development of diabetes insipidus vary depending on the type of | The risk factors in the development of diabetes insipidus vary depending on the type of diabetes insipidus being described. There are a few risk factors in the development of central diabetes which include [[genetic mutations]], [[Pituitary disease|pituitary disorders]], [[Hypothalamic dysfunction|hypothalamic injury,]] head [[tumors]]. The most potent risk factor in the development of [[nephrogenic diabetes insipidus]] is [[lithium]] use as [[lithium]] has a very narrow [[therapeutic index]] of 0.4-0.8. Excessive water intake has been identified to be the only risk factor associated with psychogenic diabetes insipidus and pregnancy for gestational diabetes insipidus.<ref name="pmid15806465">{{cite journal |vauthors=Garofeanu CG, Weir M, Rosas-Arellano MP, Henson G, Garg AX, Clark WF |title=Causes of reversible nephrogenic diabetes insipidus: a systematic review |journal=Am. J. Kidney Dis. |volume=45 |issue=4 |pages=626–37 |year=2005 |pmid=15806465 |doi= |url=}}</ref> | ||
==Risk Factors== | ==Risk Factors== | ||
*Genetic risk factors<ref name="pmid10749568">{{cite journal |vauthors=Morello JP, Salahpour A, Laperrière A, Bernier V, Arthus MF, Lonergan M, Petäjä-Repo U, Angers S, Morin D, Bichet DG, Bouvier M |title=Pharmacological chaperones rescue cell-surface expression and function of misfolded V2 vasopressin receptor mutants |journal=J. Clin. Invest. |volume=105 |issue=7 |pages=887–95 |year=2000 |pmid=10749568 |pmc=377482 |doi=10.1172/JCI8688 |url=}}</ref> | *[[Genetic]] risk factors<ref name="pmid10749568">{{cite journal |vauthors=Morello JP, Salahpour A, Laperrière A, Bernier V, Arthus MF, Lonergan M, Petäjä-Repo U, Angers S, Morin D, Bichet DG, Bouvier M |title=Pharmacological chaperones rescue cell-surface expression and function of misfolded V2 vasopressin receptor mutants |journal=J. Clin. Invest. |volume=105 |issue=7 |pages=887–95 |year=2000 |pmid=10749568 |pmc=377482 |doi=10.1172/JCI8688 |url=}}</ref> | ||
*Polycystic Kidney Disease<ref name="pmid15153548">{{cite journal |vauthors=Devonald MA, Karet FE |title=Renal epithelial traffic jams and one-way streets |journal=J. Am. Soc. Nephrol. |volume=15 |issue=6 |pages=1370–81 |year=2004 |pmid=15153548 |doi= |url=}}</ref> | *[[Polycystic kidney disease|Polycystic Kidney Disease]]<ref name="pmid15153548">{{cite journal |vauthors=Devonald MA, Karet FE |title=Renal epithelial traffic jams and one-way streets |journal=J. Am. Soc. Nephrol. |volume=15 |issue=6 |pages=1370–81 |year=2004 |pmid=15153548 |doi= |url=}}</ref> | ||
*Pituitary Disorders<ref name="pmid16713495">{{cite journal |vauthors=Bichet DG |title=Hereditary polyuric disorders: new concepts and differential diagnosis |journal=Semin. Nephrol. |volume=26 |issue=3 |pages=224–33 |year=2006 |pmid=16713495 |doi=10.1016/j.semnephrol.2006.02.004 |url=}}</ref> | *[[Pituitary disease|Pituitary Disorders]]<ref name="pmid16713495">{{cite journal |vauthors=Bichet DG |title=Hereditary polyuric disorders: new concepts and differential diagnosis |journal=Semin. Nephrol. |volume=26 |issue=3 |pages=224–33 |year=2006 |pmid=16713495 |doi=10.1016/j.semnephrol.2006.02.004 |url=}}</ref> | ||
*Hypothalamic injury | *[[Hypothalamic dysfunction|Hypothalamic injury]] | ||
*Hypercalcemia | *[[Hypercalcemia]] | ||
*Head Tumors<ref name="pmid10477148">{{cite journal |vauthors=van Lieburg AF, Knoers NV, Monnens LA |title=Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus |journal=J. Am. Soc. Nephrol. |volume=10 |issue=9 |pages=1958–64 |year=1999 |pmid=10477148 |doi= |url=}}</ref> | *Head [[Tumors]]<ref name="pmid10477148">{{cite journal |vauthors=van Lieburg AF, Knoers NV, Monnens LA |title=Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus |journal=J. Am. Soc. Nephrol. |volume=10 |issue=9 |pages=1958–64 |year=1999 |pmid=10477148 |doi= |url=}}</ref> | ||
*Pregnancy | *[[Pregnancy]] | ||
*Sickle cell disease | *[[Sickle-cell disease|Sickle cell disease]] | ||
*Amyloidosis<ref name="pmid26077742">{{cite journal |vauthors=Bockenhauer D, Bichet DG |title=Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus |journal=Nat Rev Nephrol |volume=11 |issue=10 |pages=576–88 |year=2015 |pmid=26077742 |doi=10.1038/nrneph.2015.89 |url=}}</ref> | *[[Amyloidosis]]<ref name="pmid26077742">{{cite journal |vauthors=Bockenhauer D, Bichet DG |title=Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus |journal=Nat Rev Nephrol |volume=11 |issue=10 |pages=576–88 |year=2015 |pmid=26077742 |doi=10.1038/nrneph.2015.89 |url=}}</ref> | ||
*Male Gender- some types of nephrogenic | *Male Gender- some types of [[nephrogenic diabetes insipidus]] have a male predisposition i.e diabetes insipidus caused by [[Aquaporin 2|AQP2]] mutations | ||
*Family History of | *Family History of [[nephrogenic diabetes insipidus]] | ||
*Excessive water consumption | *Excessive water consumption | ||
*pregnancy | *[[pregnancy]] | ||
==References== | ==References== |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
The risk factors in the development of diabetes insipidus vary depending on the type of diabetes insipidus being described. There are a few risk factors in the development of central diabetes which include genetic mutations, pituitary disorders, hypothalamic injury, head tumors. The most potent risk factor in the development of nephrogenic diabetes insipidus is lithium use as lithium has a very narrow therapeutic index of 0.4-0.8. Excessive water intake has been identified to be the only risk factor associated with psychogenic diabetes insipidus and pregnancy for gestational diabetes insipidus.[1]
Risk Factors
- Genetic risk factors[2]
- Polycystic Kidney Disease[3]
- Pituitary Disorders[4]
- Hypothalamic injury
- Hypercalcemia
- Head Tumors[5]
- Pregnancy
- Sickle cell disease
- Amyloidosis[6]
- Male Gender- some types of nephrogenic diabetes insipidus have a male predisposition i.e diabetes insipidus caused by AQP2 mutations
- Family History of nephrogenic diabetes insipidus
- Excessive water consumption
- pregnancy
References
- ↑ Garofeanu CG, Weir M, Rosas-Arellano MP, Henson G, Garg AX, Clark WF (2005). "Causes of reversible nephrogenic diabetes insipidus: a systematic review". Am. J. Kidney Dis. 45 (4): 626–37. PMID 15806465.
- ↑ Morello JP, Salahpour A, Laperrière A, Bernier V, Arthus MF, Lonergan M, Petäjä-Repo U, Angers S, Morin D, Bichet DG, Bouvier M (2000). "Pharmacological chaperones rescue cell-surface expression and function of misfolded V2 vasopressin receptor mutants". J. Clin. Invest. 105 (7): 887–95. doi:10.1172/JCI8688. PMC 377482. PMID 10749568.
- ↑ Devonald MA, Karet FE (2004). "Renal epithelial traffic jams and one-way streets". J. Am. Soc. Nephrol. 15 (6): 1370–81. PMID 15153548.
- ↑ Bichet DG (2006). "Hereditary polyuric disorders: new concepts and differential diagnosis". Semin. Nephrol. 26 (3): 224–33. doi:10.1016/j.semnephrol.2006.02.004. PMID 16713495.
- ↑ van Lieburg AF, Knoers NV, Monnens LA (1999). "Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus". J. Am. Soc. Nephrol. 10 (9): 1958–64. PMID 10477148.
- ↑ Bockenhauer D, Bichet DG (2015). "Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus". Nat Rev Nephrol. 11 (10): 576–88. doi:10.1038/nrneph.2015.89. PMID 26077742.