Hypoaldosteronism diagnostic criteria: Difference between revisions
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*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. | *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. | ||
**In these patients [[Plasma renin activity|plasma renin activity (PRA)]], serum [[aldosterone]], and serum [[cortisol]] should be measured. | **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, serum mineralocorticoid, corticosteroid and androgen level. | **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. | **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 NSAID, ACEi, B blockers, heparin, calcineurin inhibitors. | *Complete history should also be obtained regarding [[drug]] use which can affect [[Aldosterone antagonist|aldosterone]] [[synthesis]] or [[Function (biology)|function]] such as [[NSAIDs|NSAID]], [[Angiotensin-converting enzyme|ACEi]], [[Beta blockers|B blockers]], [[heparin]], [[Calcineurin inhibitor|calcineurin inhibitors]]. | ||
*Asymptomatic hypoaldosteronism can also be discovered during routine laboratory evaluations. | *Asymptomatic hypoaldosteronism can also be discovered during routine [[laboratory]] evaluations. | ||
==References== | ==References== | ||
Revision as of 15:21, 31 August 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.
- 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 NSAID, ACEi, B blockers, heparin, calcineurin inhibitors.
- Asymptomatic hypoaldosteronism can also be discovered during routine laboratory evaluations.