Hypoaldosteronism diagnostic criteria: Difference between revisions
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{{Hypoaldosteronism}} | {{Hypoaldosteronism}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}}{{Akshun}} | ||
==Overview== | ==Overview== | ||
There is no established criteria for the diagnosis of hypoaldosteronism. | There is no established [[criteria]] for the [[diagnosis]] of hypoaldosteronism. However, a positive history of [[hypotension]], [[muscle weakness]] and [[fatigue]] should raise suspicion for hypoaldosteronism. These [[patients]] should first be tested for [[serum]] [[potassium]] levels and later for [[Plasma renin activity|plasma renin activity (PRA)]], serum [[aldosterone]], and serum [[cortisol]]. [[Asymptomatic]] hypoaldosteronism can also be discovered on routine [[laboratory]] evaluations. | ||
==Diagnostic Criteria== | ==Diagnostic Criteria== | ||
*There is no established criteria for the diagnosis of hypoaldosteronism. However, patients with suspected hypoaldosteronism should be tested for underlying conditions which can lead to decreased aldosterone level or aldosterone resistance such as diabetes, chronic kidney disease, serum mineralocorticoid, corticosteroid and androgen level. | *There is no established [[criteria]] for the [[diagnosis]] of hypoaldosteronism. However, a positive history of [[hypotension]], [[muscle weakness]] and [[fatigue]] should raise suspicion for hypoaldosteronism.<ref name="pmid9300202">{{cite journal |vauthors=White PC |title=Abnormalities of aldosterone synthesis and action in children |journal=Curr. Opin. Pediatr. |volume=9 |issue=4 |pages=424–30 |year=1997 |pmid=9300202 |doi= |url=}}</ref><ref name="pmid10559665">{{cite journal |vauthors=Peter M, Dubuis JM, Sippell WG |title=Disorders of the aldosterone synthase and steroid 11beta-hydroxylase deficiencies |journal=Horm. Res. |volume=51 |issue=5 |pages=211–22 |year=1999 |pmid=10559665|url=}}</ref><ref name="pmid16024935">{{cite journal |vauthors=Kuribayashi I, Nomoto S, Massa G, Oostdijk W, Wit JM, Wolffenbuttel BH, Shizuta Y, Honke K |title=Steroid 11-beta-hydroxylase deficiency caused by compound heterozygosity for a novel mutation, p.G314R, in one CYP11B1 allele, and a chimeric CYP11B2/CYP11B1 in the other allele |journal=Horm. Res. |volume=63 |issue=6 |pages=284–93 |year=2005 |pmid=16024935 |doi=10.1159/000087074 |url=}}</ref> | ||
**In these patients [[Plasma renin activity|plasma renin activity (PRA)]], serum [[aldosterone]], and serum [[cortisol]] should be measured. | |||
**Patients with suspected hypoaldosteronism should be also be tested for underlying conditions which can lead to decreased [[aldosterone]] level or [[aldosterone]] resistance such as [[diabetes]], [[chronic kidney disease]], [[Mineralocorticoid|serum mineralocorticoid]], [[corticosteroid]] and [[androgen]] level. | |||
**Patients with [[family history]] of hypoaldosteronism should be checked for [[CYP11B2]] ([[aldosterone synthase]]) and NR3C2 ([[mineralocorticoid receptor]]) [[gene]] [[mutations]]. | |||
*Complete history should also be obtained regarding [[drug]] use which can affect [[Aldosterone antagonist|aldosterone]] [[synthesis]] or [[Function (biology)|function]] such as [[NSAIDs]], [[ACE inhibitors]], [[beta blockers]], [[heparin]], [[Calcineurin inhibitor|calcineurin inhibitors]].<ref name="pmid21883995">{{cite journal |vauthors=Raebel MA |title=Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers |journal=Cardiovasc Ther |volume=30 |issue=3 |pages=e156–66 |year=2012 |pmid=21883995 |doi=10.1111/j.1755-5922.2010.00258.x |url=}}</ref><ref name="pmid19707264">{{cite journal |vauthors=Sadjadi SA, McMillan JI, Jaipaul N, Blakely P, Hline SS |title=A comparative study of the prevalence of hyperkalemia with the use of angiotensin-converting enzyme inhibitors versus angiotensin receptor blockers |journal=Ther Clin Risk Manag |volume=5 |issue=3 |pages=547–52 |year=2009 |pmid=19707264 |pmc=2710386 |doi= |url=}}</ref> | |||
*Asymptomatic hypoaldosteronism can also be discovered during routine [[laboratory]] evaluations.<ref name="pmid776486">{{cite journal |vauthors=Hirschman GH, Rao DD, Oyemade O, Chan JC |title=Renal tubular acidosis: practical guides to diagnosis and treatment |journal=Clin Pediatr (Phila) |volume=15 |issue=7 |pages=645–50 |year=1976 |pmid=776486 |doi=10.1177/000992287601500716 |url=}}</ref> | |||
==References== | ==References== | ||
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{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Disease]] | |||
[[Category:Endocrinology]] | |||
[[Category:Nephrology]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Medicine]] | |||
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Latest revision as of 16:39, 18 October 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
Overview
There is no established criteria for the diagnosis of hypoaldosteronism. However, a positive history of hypotension, muscle weakness and fatigue should raise suspicion for hypoaldosteronism. These patients should first be tested for serum potassium levels and later for plasma renin activity (PRA), serum aldosterone, and serum cortisol. Asymptomatic hypoaldosteronism can also be discovered on routine laboratory evaluations.
Diagnostic Criteria
- There is no established criteria for the diagnosis of hypoaldosteronism. However, a positive history of hypotension, muscle weakness and fatigue should raise suspicion for hypoaldosteronism.[1][2][3]
- In these patients plasma renin activity (PRA), serum aldosterone, and serum cortisol should be measured.
- Patients with suspected hypoaldosteronism should be also be tested for underlying conditions which can lead to decreased aldosterone level or aldosterone resistance such as diabetes, chronic kidney disease, serum mineralocorticoid, corticosteroid and androgen level.
- Patients with family history of hypoaldosteronism should be checked for CYP11B2 (aldosterone synthase) and NR3C2 (mineralocorticoid receptor) gene mutations.
- Complete history should also be obtained regarding drug use which can affect aldosterone synthesis or function such as NSAIDs, ACE inhibitors, beta blockers, heparin, calcineurin inhibitors.[4][5]
- Asymptomatic hypoaldosteronism can also be discovered during routine laboratory evaluations.[6]
References
- ↑ White PC (1997). "Abnormalities of aldosterone synthesis and action in children". Curr. Opin. Pediatr. 9 (4): 424–30. PMID 9300202.
- ↑ Peter M, Dubuis JM, Sippell WG (1999). "Disorders of the aldosterone synthase and steroid 11beta-hydroxylase deficiencies". Horm. Res. 51 (5): 211–22. PMID 10559665.
- ↑ Kuribayashi I, Nomoto S, Massa G, Oostdijk W, Wit JM, Wolffenbuttel BH, Shizuta Y, Honke K (2005). "Steroid 11-beta-hydroxylase deficiency caused by compound heterozygosity for a novel mutation, p.G314R, in one CYP11B1 allele, and a chimeric CYP11B2/CYP11B1 in the other allele". Horm. Res. 63 (6): 284–93. doi:10.1159/000087074. PMID 16024935.
- ↑ Raebel MA (2012). "Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers". Cardiovasc Ther. 30 (3): e156–66. doi:10.1111/j.1755-5922.2010.00258.x. PMID 21883995.
- ↑ Sadjadi SA, McMillan JI, Jaipaul N, Blakely P, Hline SS (2009). "A comparative study of the prevalence of hyperkalemia with the use of angiotensin-converting enzyme inhibitors versus angiotensin receptor blockers". Ther Clin Risk Manag. 5 (3): 547–52. PMC 2710386. PMID 19707264.
- ↑ Hirschman GH, Rao DD, Oyemade O, Chan JC (1976). "Renal tubular acidosis: practical guides to diagnosis and treatment". Clin Pediatr (Phila). 15 (7): 645–50. doi:10.1177/000992287601500716. PMID 776486.