Hypoaldosteronism medical therapy: Difference between revisions

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==Overview==
==Overview==
The mainstay of treatment for hypoaldosteronism depends upon the level of plasma [[potassium]]. Prompt [[ECG]] is advised in all [[patients]] suspected of hypoaldosteronism as [[hyperkalemia]] may lead to [[Conduction disorders|cardiac conduction defects]] and life threatening [[arrhythmias]]. Patients with no [[ECG]] changes and moderate [[hyperkalemia]] (6.5–7.5 mmol/l) require only monitoring. Patients with severe [[hyperkalemia]] (>7.5 mmol/l) are treated with [[emergency]] measures for [[hyperkalemia]] ([[calcium]], [[insulin]], β<sub>2</sub> agonist or cation resins) and [[fludrocortisone]]. Depending upon the [[volume status]], [[patients]] may be treated with either [[Normal saline|0.9% normal saline]] ([[hypovolemia]]) or [[furosemide]] ([[Hypervolemia|hypervolemic]]).
The mainstay of treatment for hypoaldosteronism depends upon the level of plasma [[potassium]]. Prompt [[ECG]] is advised in all [[patients]] suspected of hypoaldosteronism as [[hyperkalemia]] may lead to [[Conduction disorders|cardiac conduction defects]] and life threatening [[arrhythmias]]. Patients with no [[ECG]] changes and moderate [[hyperkalemia]] (6.5–7.5 mmol/l) require only monitoring. Patients with severe [[hyperkalemia]] (>7.5 mmol/l) are treated with [[emergency]] measures for [[hyperkalemia]] ([[calcium]], [[insulin]], [[Beta2-adrenergic receptor agonist|β<sub>2</sub> agonist]] or cation resins) and [[fludrocortisone]]. Depending upon the [[volume status]], [[patients]] may be treated with either [[Normal saline|0.9% normal saline]] ([[hypovolemia]]) or [[furosemide]] ([[Hypervolemia|hypervolemic]]).


==Medical Therapy==
==Medical Therapy==
[[Medical]] [[therapy]] for hypoaldosteronism depends upon the [[age]] of the [[patient]] and other concurrent [[disorders]] such as [[diabetic nephropathy]] and [[renal insufficiency]]. [[Medical]] [[therapy]] includes: <ref name="pmid24944031">{{cite journal| author=Magill SB| title=Pathophysiology, diagnosis, and treatment of mineralocorticoid disorders. | journal=Compr Physiol | year= 2014 | volume= 4 | issue= 3 | pages= 1083-119 | pmid=24944031 | doi=10.1002/cphy.c130042 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24944031  }} </ref><ref name="pmid8928409">{{cite journal |vauthors=Hrnciar J |title=[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism] |language=Slovak |journal=Vnitr Lek |volume=42 |issue=6 |pages=394–9 |year=1996 |pmid=8928409 |doi= |url=}}</ref><ref name="pmid4604546">{{cite journal |vauthors=Ettinger PO, Regan TJ, Oldewurtel HA |title=Hyperkalemia, cardiac conduction, and the electrocardiogram: a review |journal=Am. Heart J. |volume=88 |issue=3 |pages=360–71 |year=1974 |pmid=4604546 |doi= |url=}}</ref>
[[Medical]] [[therapy]] for hypoaldosteronism depends upon the [[age]] of the [[patient]] and other concurrent [[disorders]] such as [[diabetic nephropathy]] and [[renal insufficiency]]. [[Medical]] [[therapy]] includes: <ref name="pmid24944031">{{cite journal| author=Magill SB| title=Pathophysiology, diagnosis, and treatment of mineralocorticoid disorders. | journal=Compr Physiol | year= 2014 | volume= 4 | issue= 3 | pages= 1083-119 | pmid=24944031 | doi=10.1002/cphy.c130042 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24944031  }} </ref><ref name="pmid8928409">{{cite journal |vauthors=Hrnciar J |title=[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism] |language=Slovak |journal=Vnitr Lek |volume=42 |issue=6 |pages=394–9 |year=1996 |pmid=8928409 |doi= |url=}}</ref><ref name="pmid4604546">{{cite journal |vauthors=Ettinger PO, Regan TJ, Oldewurtel HA |title=Hyperkalemia, cardiac conduction, and the electrocardiogram: a review |journal=Am. Heart J. |volume=88 |issue=3 |pages=360–71 |year=1974 |pmid=4604546 |doi= |url=}}</ref>
*Prompt [[ECG]] must be obtained in all suspected [[patients]] of hypoaldosteronism as [[hyperkalemia]] may alter the [[Electrical conduction system of the heart|electrical activity of heart]] and predispose to life threatening [[arrhythmias]]
*Prompt [[ECG]] must be obtained in all suspected [[patients]] of hypoaldosteronism as [[hyperkalemia]] may alter the [[Electrical conduction system of the heart|electrical activity of heart]] and predispose to life threatening [[arrhythmias]].
*Patients with no [[ECG]] changes and moderate [[hyperkalemia]] (6.5–7.5 mmol/l) require only monitoring [[potassium]] [[concentrations]].
*Patients with no [[ECG]] changes and moderate [[hyperkalemia]] (6.5–7.5 mmol/l) require only monitoring [[potassium]] [[concentrations]].
**[[Drugs]] promoting [[hyperkalemia]] should be avoided, such as [[Beta blockers|β blockers]], [[ACE inhibitor]], [[angiotensin receptor blockers]] and [[potassium-sparing diuretics]].
**[[Drugs]] promoting [[hyperkalemia]] should be avoided, such as [[Beta blockers|β blockers]], [[ACE inhibitor]], [[angiotensin receptor blockers]] and [[potassium-sparing diuretics]].
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*: '''Note:''' Usually infused through a [[central venous catheter]] as the [[calcium]] may cause [[phlebitis]] and does not lower [[potassium]] but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]].
*: '''Note:''' Usually infused through a [[central venous catheter]] as the [[calcium]] may cause [[phlebitis]] and does not lower [[potassium]] but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]].
* '''1.2 [[Insulin]]'''  
* '''1.2 [[Insulin]]'''  
** Preferred regimen (1): Short acting [[insulin]] (e.g. Actrapid) 10-15u IV along with 50ml of 50% dextrose (to prevent [[hypoglycemia]])  
** Preferred regimen (1): Short acting [[insulin]] (e.g. [[Actrapid]]) 10-15 u IV along with 50 ml of 50% dextrose (to prevent [[hypoglycemia]])  
*: '''Note:''' Short acting Insulin leads to a shift of [[potassium]] ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]].
*: '''Note:''' Short acting Insulin leads to a shift of [[potassium]] ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]].
* '''1.3 [[Bicarbonate]] therapy'''
* '''1.3 [[Bicarbonate]] therapy'''
** Preferred regimen (1): [[Sodium bicarbonate]] 1 [[ampule]] (45mEq) infused over 5 minutes) is effective in cases of [[metabolic acidosis]].
** Preferred regimen (1): [[Sodium bicarbonate]] 1 [[ampule]] (45mEq) infused over 5 minutes is effective in cases of [[metabolic acidosis]].
*: '''Note:'''The [[bicarbonate]] ion will stimulate an exchange of cellular H<sup>+</sup> for Na<sup>+</sup>, thus leading to stimulation of the [[sodium-potassium ATPase]].
*: '''Note:'''The [[bicarbonate]] ion will stimulate an exchange of cellular H<sup>+</sup> for Na<sup>+</sup>, thus leading to stimulation of the [[sodium-potassium ATPase]].
* '''1.4  β<sub>2</sub>-selective agonist'''
* '''1.4  β<sub>2</sub>-selective agonist'''
** Preferred regimen (1): [[Salbutamol]] nebulization (e.g. 10-20 mg)
** Preferred regimen (1): [[Salbutamol]] [[nebulization]] (e.g. 10-20 mg)
** Preferred regimen (2): ([[Albuterol]], [[Ventolin]]<sup>®</sup>)  nebulization (e.g. 10-20 mg)  
** Preferred regimen (2): ([[Albuterol]], [[Ventolin]]<sup>®</sup>)  [[nebulization]] (e.g. 10-20 mg)  
*: '''Note:''' This [[drug]] promotes movement of [[potassium]] into [[cells]], lowering the blood levels.
*: '''Note:''' This [[drug]] promotes movement of [[potassium]] into [[cells]], lowering the [[blood]] levels.
* '''1.5 Potassium binding resins'''
* '''1.5 Potassium binding resins'''
** Preferred regimen (1): [[Polystyrene sulfonate]] (calcium resonium, [[kayexalate]]) is a binding resin that binds [[potassium]] within the [[Intestines|intestine]] and removes it from the [[body]] by [[defecation]].  
** Preferred regimen (1): [[Polystyrene sulfonate]] (calcium resonium, [[kayexalate]]) is a binding resin that binds [[potassium]] within the [[Intestines|intestine]] and removes it from the [[body]] by [[defecation]].  
** Preferred regimen (2): Calcium resonium (15g three times a day in water) can be given by [[mouth]].
** Preferred regimen (2): [[Calcium resonium]] (15g three times a day in water) can be given by [[mouth]].
** Preferred regimen (3): [[Kayexalate]] can be given by [[mouth]] or as an [[enema]]. In both cases, the resin absorbs [[potassium]] within the [[Intestines|intestine]] and carries it out of the body by [[defecation]].
** Preferred regimen (3): [[Kayexalate]] can be given by [[mouth]] or as an [[enema]]. In both cases, the resin absorbs [[potassium]] within the [[Intestines|intestine]] and carries it out of the body by [[defecation]].
** Preferred regimen (4): [[Patiromer]] [[anion]]  
** Preferred regimen (4): [[Patiromer]] [[anion]]  
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**'''2.1.1 [[Thiazide diuretics]]:'''
**'''2.1.1 [[Thiazide diuretics]]:'''
***Preferred regimen (1): [[furosemide]] 20 to 40 mg 24h
***Preferred regimen (1): [[furosemide]] 20 to 40 mg 24h
**:'''Note:''' Diuretics are the first-line therapy for [[patients]] with severe [[hyperkalemia]] (>7.5 mmol/l) and [[fluid overload]] (seen in [[renal]] impairment or [[congestive heart failure]]). Avoid [[diuretics]] in [[patients]] with [[signs]] of [[hypotension]] or [[volume depletion]].
**:'''Note:''' [[Diuretics]] are the first-line therapy for [[patients]] with severe [[hyperkalemia]] (>7.5 mmol/l) and [[fluid overload]] (seen in [[renal]] impairment or [[congestive heart failure]]). Avoid [[diuretics]] in [[patients]] with [[signs]] of [[hypotension]] or [[volume depletion]].
**2.1.2 [[Patients]] who are unable to tolerate [[diuretics]] due to underlying [[hypotension]] or [[volume depletion]] are treated with:
**2.1.2 [[Patients]] who are unable to tolerate [[diuretics]] due to underlying [[hypotension]] or [[volume depletion]] are treated with:
***Preferred regimen (1): [[Sodium bicarbonate]] (NaHCO3)   
***Preferred regimen (1): [[Sodium bicarbonate]] (NaHCO3)   
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** '''2.3.1 [[Aldosterone]] analogues:'''
** '''2.3.1 [[Aldosterone]] analogues:'''
**: Preferred regime (1): 9α-[[fludrocortisone]] 0.05 to 0.2 mg q24h
**: Preferred regime (1): 9α-[[fludrocortisone]] 0.05 to 0.2 mg q24h
**: Note (1): Isolated hypoaldosteronism from [[CYP11B2]] [[gene]] [[mutation]] presents in [[infancy]] and are treated with 9α-[[fludrocortisone]].
**: '''Note (1):''' Isolated hypoaldosteronism from [[CYP11B2]] [[gene]] [[mutation]] presents in [[infancy]] and are treated with 9α-[[fludrocortisone]].
**: Note (2): In adults treatment is not necessary.<ref name="pmid26981183" />
**: '''Note (2):''' In adults treatment is not necessary.<ref name="pmid26981183" />


* '''2.4 Pseudohypoaldosteronism type I''': Patients of [[pseudohypoaldosteronism]] are resistant to [[aldosterone]] or [[mineralocorticoid]] therapy and treatment is based on:<ref name="pmid28484659">{{cite journal |vauthors=Nur N, Lang C, Hodax JK, Quintos JB |title=Systemic Pseudohypoaldosteronism Type I: A Case Report and Review of the Literature |journal=Case Rep Pediatr |volume=2017 |issue= |pages=7939854 |year=2017 |pmid=28484659 |pmc=5412170 |doi=10.1155/2017/7939854 |url=}}</ref>
* '''2.4 Pseudohypoaldosteronism type I''': Patients of [[pseudohypoaldosteronism]] are resistant to [[aldosterone]] or [[mineralocorticoid]] therapy and treatment is based on:<ref name="pmid28484659">{{cite journal |vauthors=Nur N, Lang C, Hodax JK, Quintos JB |title=Systemic Pseudohypoaldosteronism Type I: A Case Report and Review of the Literature |journal=Case Rep Pediatr |volume=2017 |issue= |pages=7939854 |year=2017 |pmid=28484659 |pmc=5412170 |doi=10.1155/2017/7939854 |url=}}</ref>

Revision as of 18:48, 26 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

The mainstay of treatment for hypoaldosteronism depends upon the level of plasma potassium. Prompt ECG is advised in all patients suspected of hypoaldosteronism as hyperkalemia may lead to cardiac conduction defects and life threatening arrhythmias. Patients with no ECG changes and moderate hyperkalemia (6.5–7.5 mmol/l) require only monitoring. Patients with severe hyperkalemia (>7.5 mmol/l) are treated with emergency measures for hyperkalemia (calcium, insulin, β2 agonist or cation resins) and fludrocortisone. Depending upon the volume status, patients may be treated with either 0.9% normal saline (hypovolemia) or furosemide (hypervolemic).

Medical Therapy

Medical therapy for hypoaldosteronism depends upon the age of the patient and other concurrent disorders such as diabetic nephropathy and renal insufficiency. Medical therapy includes: [1][2][3]

1. Management of Hyperkalemia

2. Management on the basis of subtype of hypoaldosteronism

  • 2.2 Hyperreninemic hypoaldosteronism: Secondary isolated hypoaldosteronism also known as hyperreninemic hypoaldosteronism is seen in patients with severe underlying illness such as liver cirrhosis or heart failure.[7]
    • 2.2.1: The primary focus of the treatment in hyperreninemic hypoaldosteronism is to treat the underlying condition.
    • 2.2.2: Decreased level of aldosterone in patients of hyperreninemic hypoaldosteronism does not lead to any clinical complications and is therefore seldom treated.

For complete therapy in adrenal insufficiency please click here.

References

  1. Magill SB (2014). "Pathophysiology, diagnosis, and treatment of mineralocorticoid disorders". Compr Physiol. 4 (3): 1083–119. doi:10.1002/cphy.c130042. PMID 24944031.
  2. Hrnciar J (1996). "[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]". Vnitr Lek (in Slovak). 42 (6): 394–9. PMID 8928409.
  3. Ettinger PO, Regan TJ, Oldewurtel HA (1974). "Hyperkalemia, cardiac conduction, and the electrocardiogram: a review". Am. Heart J. 88 (3): 360–71. PMID 4604546.
  4. Kaisar MO, Wiggins KJ, Sturtevant JM, Hawley CM, Campbell SB, Isbel NM, Mudge DW, Bofinger A, Petrie JJ, Johnson DW (2006). "A randomized controlled trial of fludrocortisone for the treatment of hyperkalemia in hemodialysis patients". Am. J. Kidney Dis. 47 (5): 809–14. doi:10.1053/j.ajkd.2006.01.014. PMID 16632019.
  5. Singhal PC, Desroches L, Mattana J, Abramovici M, Wagner JD, Maesaka JK (1993). "Mineralocorticoid therapy lowers serum potassium in patients with end-stage renal disease". Am. J. Nephrol. 13 (2): 138–41. PMID 8342580.
  6. Tan SY, Burton M (1981). "Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia". Arch. Intern. Med. 141 (1): 30–3. PMID 7004370.
  7. Aguilera G, Fujita K, Catt KJ (1981). "Mechanisms of inhibition of aldosterone secretion by adrenocorticotropin". Endocrinology. 108 (2): 522–8. doi:10.1210/endo-108-2-522. PMID 6256154.
  8. 8.0 8.1 Sousa AG, Cabral JV, El-Feghaly WB, de Sousa LS, Nunes AB (2016). "Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management". World J Diabetes. 7 (5): 101–11. doi:10.4239/wjd.v7.i5.101. PMC 4781902. PMID 26981183.
  9. Nur N, Lang C, Hodax JK, Quintos JB (2017). "Systemic Pseudohypoaldosteronism Type I: A Case Report and Review of the Literature". Case Rep Pediatr. 2017: 7939854. doi:10.1155/2017/7939854. PMC 5412170. PMID 28484659.
  10. Maesaka JK, Imbriano LJ, Miyawaki N (2017). "Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia". World J Nephrol. 6 (2): 59–71. doi:10.5527/wjn.v6.i2.59. PMC 5339638. PMID 28316939.

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