Hypoaldosteronism medical therapy: Difference between revisions

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{{Hypoaldosteronism}}
{{Hypoaldosteronism}}
 
{{CMG}}; {{AE}}{{SSW}}{{Akshun}}
{{CMG}}; {{AE}}{{Akshun}}


==Overview==
==Overview==
The mainstay of treatment for hypoaldosteronism depends upon the level of plasma potassium. Prompt ECG is advised in all suspected patients of hypoaldosteronism as hyperkalemia can lead to cardiac conduction defects. 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 fludrocortisone. Depending upon the volume status, patients may be treated with either 0.9% normal saline or furosemide.
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 should be obtained in all suspected patients of hypoaldosteronism as hyperkalemia may alter the electrical activity of heart and predispose to cardiac conduction defects.
*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 β blockers, ACEi, ARB 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]].
**Reduced dietary intake of potassium.
**Reduced [[dietary]] intake of [[potassium]].
*Patients with severe hyperkalemia (>7.5 mmol/l) are treated with emergency measures for hyperkalemia as necessary (see below) and fludrocortisone 0.05 to 0.1 mg PO qd.
*Patients with severe [[hyperkalemia]] (>7.5 mmol/l) are treated with [[emergency]] measures for [[hyperkalemia]] as necessary (see below) and [[fludrocortisone]] 0.05 to 0.1 mg PO q24h.
*Depending upon the volume status, patients may be treated with:  
*Depending upon the [[volume status]], patients may be treated with:  
**In hypovolemic patients, normal saline 0.9% is given to restore volume status.
**In [[Hypovolemia|hypovolemic]] [[patients]], [[Normal saline|normal saline 0.9%]] is given to restore [[volume status]].
**In hypervolemic patients (signs of volume overload) or underlying heart failure furosemide 20 to 40 mg qd is given.
**In [[Hypervolemia|hypervolemic]] [[patients]] (signs of volume overload) or underlying [[heart failure]], [[furosemide]] 20 to 40 mg q24h is given.
 
'''1. Management of Hyperkalemia'''
===Management of Hyperkalemia===
* '''1.1 [[Calcium]] supplementation'''
* [[Calcium]] supplementation (calcium gluconate 10% (10ml), preferably through a [[central venous catheter]] as the calcium may cause [[phlebitis]]) does not lower potassium but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]].
** Preferred regimen (1): [[Calcium gluconate]] 10% (10ml)
* [[Insulin]] (e.g. intravenous injection of 10-15u of (short acting) insulin (e.g. Actrapid) {along with 50ml of 50% dextrose to prevent hypoglycemia}) will lead to a shift of potassium ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]].
*: '''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]].
* [[Bicarbonate]] therapy (e.g. 1 ampule (45mEq) infused over 5 minutes) is effective in cases of metabolic acidosis. 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]].
* '''1.2 [[Insulin]]'''
* [[Salbutamol]] (albuterol, Ventolin<sup>®</sup>) is a β<sub>2</sub>-selective catacholamine that is administered by nebuliser (e.g. 10-20 mg).  This drug promotes movement of K into cells, lowering the blood levels.
** Preferred regimen (1): Short acting [[insulin]] (e.g. [[Actrapid]]) 10-15 u IV along with 50 ml of 50% dextrose (to prevent [[hypoglycemia]])  
* [[Polystyrene sulfonate]] (Calcium Resonium, Kayexalate) is a binding resin that binds K within the intestine and removes it from the body by defecation. Calcium Resonium (15g three times a day in water) can be given by mouth. Kayexelate can be given by mouth or as an [[enema]]. In both cases, the resin absorbs K within the intestine and carries it out of the body by [[defecation]].  This medication may cause diarrhea.
*: '''Note:''' Short acting Insulin leads to a shift of [[potassium]] ions into cells, secondary to increased activity of the [[sodium-potassium ATPase]].
* Refractory or severe cases may need [[dialysis]] to remove the potassium from the circulation.
* '''1.3 [[Bicarbonate]] therapy'''
* Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a [[diuretic]] (such as [[furosemide]] (Lasix<sup>®</sup>) or [[hydrochlorothiazide]]).
** Preferred regimen (1): [[Sodium bicarbonate]] 1 [[ampule]] (45mEq) infused over 5 minutes is effective in cases of [[metabolic acidosis]].
* [[Patiromer]] anion is a potassium binding ion cation exchange polymer that increases the [[gastrointestinal]] excretion of potassium (it is available in 8.4, 16.8, and 25.2 grams of powder in packets to be administered once daily).  [[Patiromer]] should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action.  
*: '''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'''
** Preferred regimen (1): [[Salbutamol]] [[nebulization]] (e.g. 10-20 mg)
===Disease Name===
** 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.
'''Hyporeninemic Hypoaldosteronism''': Treatment is aimed at normalizing volume status, plasma potassium and aldosterone levels.<ref name="pmid16632019">{{cite journal |vauthors=Kaisar MO, Wiggins KJ, Sturtevant JM, Hawley CM, Campbell SB, Isbel NM, Mudge DW, Bofinger A, Petrie JJ, Johnson DW |title=A randomized controlled trial of fludrocortisone for the treatment of hyperkalemia in hemodialysis patients |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=809–14 |year=2006 |pmid=16632019 |doi=10.1053/j.ajkd.2006.01.014 |url=}}</ref><ref name="pmid8342580">{{cite journal |vauthors=Singhal PC, Desroches L, Mattana J, Abramovici M, Wagner JD, Maesaka JK |title=Mineralocorticoid therapy lowers serum potassium in patients with end-stage renal disease |journal=Am. J. Nephrol. |volume=13 |issue=2 |pages=138–41 |year=1993 |pmid=8342580 |doi= |url=}}</ref><ref name="pmid7004370">{{cite journal |vauthors=Tan SY, Burton M |title=Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia |journal=Arch. Intern. Med. |volume=141 |issue=1 |pages=30–3 |year=1981 |pmid=7004370 |doi= |url=}}</ref>
* '''1.5 Potassium binding resins'''
*Thiazide diuretics: Diuretics (furosemide 20 to 40 mg qd) 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.
** 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]].  
*Patients who cannot tolerate diuretics due to underlying hypotension or volume depletion are treated with:
** Preferred regimen (2): [[Calcium resonium]] (15g three times a day in water) can be given by [[mouth]].
**''Patients with normal renal function'': Sodium bicarbonate (NaHCO3) is the second line therapy and used in patients who cannot tolerate diuretics due to underlying hypotension or volume depletion. In these patients sodium bicarbonate (NaHCO3) can be used to increase distal delivery of bicarbonate anion and increase urinary potassium excretion. Sodium bicarbonate (NaHCO3) also corrects underlying metabolic acidosis.  
** 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]].
**''Patient with inadequate renal function'': Sodium polystyrene sulfonate is used in patients with underlying renal disease and decreased potassium excretion. 1gm of sodium polystyrene sulfonate can remove upto 1 mEq of potassium.
** Preferred regimen (4): [[Patiromer]] [[anion]]
*Aldosterone analogues are the third line therapy such as  fludrocortisone in the dose of 0.1-0.3 mg/day.
*: '''Note (1):''' [[Kayexalate]] may cause [[diarrhea]].
*: '''Note (2):''' [[Refractory]] or severe cases may need [[dialysis]] to remove the [[potassium]] from the [[circulation]].
*: '''Note (3):''' Preventing recurrence of [[hyperkalemia]] typically involves reduction of [[dietary]] [[potassium]], removal of an offending [[medication]], and/or the addition of a [[diuretic]] (such as [[furosemide]] (Lasix<sup>®</sup>) or [[hydrochlorothiazide]]).
*: '''Note (4):''' [[Patiromer]] [[anion]] is a [[potassium]] binding ion cation exchange polymer that increases the [[gastrointestinal]] excretion of [[potassium]] (it is available in 8.4, 16.8, and 25.2 grams of powder in packets to be administered once daily).
*: '''Note (5):''' [[Patiromer]] should not be used as an [[emergency]] treatment for life-threatening [[hyperkalemia]] because of its delayed onset of action.
'''2. Management on the basis of subtype of hypoaldosteronism'''
* '''2.1 Hyporeninemic Hypoaldosteronism''': Treatment is aimed at normalizing [[volume status]], plasma [[potassium]] and [[aldosterone]] levels.<ref name="pmid16632019">{{cite journal |vauthors=Kaisar MO, Wiggins KJ, Sturtevant JM, Hawley CM, Campbell SB, Isbel NM, Mudge DW, Bofinger A, Petrie JJ, Johnson DW |title=A randomized controlled trial of fludrocortisone for the treatment of hyperkalemia in hemodialysis patients |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=809–14 |year=2006 |pmid=16632019 |doi=10.1053/j.ajkd.2006.01.014 |url=}}</ref><ref name="pmid8342580">{{cite journal |vauthors=Singhal PC, Desroches L, Mattana J, Abramovici M, Wagner JD, Maesaka JK |title=Mineralocorticoid therapy lowers serum potassium in patients with end-stage renal disease |journal=Am. J. Nephrol. |volume=13 |issue=2 |pages=138–41 |year=1993 |pmid=8342580 |doi= |url=}}</ref><ref name="pmid7004370">{{cite journal |vauthors=Tan SY, Burton M |title=Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia |journal=Arch. Intern. Med. |volume=141 |issue=1 |pages=30–3 |year=1981 |pmid=7004370 |doi= |url=}}</ref>
**'''2.1.1 [[Thiazide diuretics]]:'''
***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]].
**'''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) 
**:'''Note:''' [[Sodium bicarbonate]] (NaHCO3) is the second line [[therapy]] and used in [[patients]] with 'normal [[renal function]] '''and''' who cannot tolerate [[diuretics]]' due to underlying [[hypotension]] or [[volume depletion]]. In these patients [[sodium bicarbonate]] (NaHCO3) can be used to increase distal delivery of [[bicarbonate]] [[anion]] and increase [[urinary]] [[potassium]] [[excretion]]. [[Sodium bicarbonate]] (NaHCO3) also corrects underlying [[metabolic acidosis]].
***Preferred regimen (2): [[Sodium polystyrene sulfonate]] 
**:'''Note:''' [[Sodium polystyrene sulfonate]] is used in patients with [[Renal function impairment|inadequate renal function]] '''and''' decreased [[potassium]] excretion. 1 gm of [[sodium polystyrene sulfonate]] can remove upto 1 mEq of [[potassium]].
**'''2.1.3 [[Aldosterone]] analogues:'''
***Preferred regimen (1): [[fludrocortisone]] 0.1-0.3 mg q24h
**:'''Note:''' [[Aldosterone]] analogues such as [[fludrocortisone]] in the dose of 0.1-0.3 mg q24h are the third line therapy .


'''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.<ref name="pmid6256154">{{cite journal |vauthors=Aguilera G, Fujita K, Catt KJ |title=Mechanisms of inhibition of aldosterone secretion by adrenocorticotropin |journal=Endocrinology |volume=108 |issue=2 |pages=522–8 |year=1981 |pmid=6256154 |doi=10.1210/endo-108-2-522 |url=}}</ref>  
* '''2.2 Hyperreninemic hypoaldosteronism''': Secondary isolated hypoaldosteronism also known as hyperreninemic hypoaldosteronism is seen in [[patients]] with severe underlying [[Illnesses|illness]] such as [[liver cirrhosis]] or [[heart failure]].<ref name="pmid6256154">{{cite journal |vauthors=Aguilera G, Fujita K, Catt KJ |title=Mechanisms of inhibition of aldosterone secretion by adrenocorticotropin |journal=Endocrinology |volume=108 |issue=2 |pages=522–8 |year=1981 |pmid=6256154 |doi=10.1210/endo-108-2-522 |url=}}</ref>
* The primary focus of the treatment in hyperreninemic hypoaldosteronism is to treat the underlying condition.  
** '''2.2.1:''' The primary focus of the treatment in hyperreninemic hypoaldosteronism is to treat the underlying condition.
* Decreased level of aldosterone in patients of hyperreninemic hypoaldosteronism does not lead to any clinical complications and is therefore seldom treated.
** '''2.2.2:''' Decreased level of [[aldosterone]] in patients of hyperreninemic hypoaldosteronism does not lead to any [[clinical]] [[complications]] and is therefore seldom treated.


'''Isolated Hypoaldosteronism''': Isolated Hypoaldosteronism from CYP11B2 gene mutation presents in infancy and are treated with 9α-fludrocortisone 0.05 to 0.2 mg daily.
* '''2.3 Isolated hypoaldosteronism''':<ref name="pmid26981183">{{cite journal| author=Sousa AG, Cabral JV, El-Feghaly WB, de Sousa LS, Nunes AB| title=Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management. | journal=World J Diabetes | year= 2016 | volume= 7 | issue= 5 | pages= 101-11 | pmid=26981183 | doi=10.4239/wjd.v7.i5.101 | pmc=4781902 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26981183  }} </ref>
In adults treatment is not necessary.<ref name="pmid26981183">{{cite journal| author=Sousa AG, Cabral JV, El-Feghaly WB, de Sousa LS, Nunes AB| title=Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management. | journal=World J Diabetes | year= 2016 | volume= 7 | issue= 5 | pages= 101-11 | pmid=26981183 | doi=10.4239/wjd.v7.i5.101 | pmc=4781902 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26981183  }} </ref>
** '''2.3.1 [[Aldosterone]] analogues:'''
**: 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 (2):''' In adults treatment is not necessary.<ref name="pmid26981183" />


'''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>
* Correcting the underlying electrolyte abnormalities with sodium chloride (2 to 8 g/day) and cation-exchange resins such as sodium polystyrene sulfonate.
** Correcting the underlying [[electrolyte abnormalities]] with [[sodium chloride]] (2 to 8 g q24h) and cation-exchange resins such as [[sodium polystyrene sulfonate]].
* Thiazide diuretics are used to treat hyperkalemia. In patients with severe hyperkalemia (>7.5 mmol/l) peritoneal dialysis may be done.
** [[Thiazide diuretics]] are used to treat [[hyperkalemia]]. In patients with severe [[hyperkalemia]] (>7.5 mmol/l) [[peritoneal dialysis]] may also be done.
* Pseudohypoaldosteronism decreases after few years and the therapy may be discontinued. However, these patients require salt supplementation till first 3-4 years of life.
** [[Pseudohypoaldosteronism]] decreases after few years and the [[therapy]] may be discontinued. However, these [[patients]] require [[salt]] supplementation till first 3-4 years of [[life]].


'''Primary or secondary adrenal insufficiency''': These patients are treated with fludrocortisone and cortisol:<ref name="pmid28316939">{{cite journal |vauthors=Maesaka JK, Imbriano LJ, Miyawaki N |title=Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia |journal=World J Nephrol |volume=6 |issue=2 |pages=59–71 |year=2017 |pmid=28316939 |pmc=5339638 |doi=10.5527/wjn.v6.i2.59 |url=}}</ref>
* '''2.5 Primary or secondary adrenal insufficiency''': These [[patients]] are treated with [[fludrocortisone]] and [[cortisol]]:<ref name="pmid28316939">{{cite journal |vauthors=Maesaka JK, Imbriano LJ, Miyawaki N |title=Application of established pathophysiologic processes brings greater clarity to diagnosis and treatment of hyponatremia |journal=World J Nephrol |volume=6 |issue=2 |pages=59–71 |year=2017 |pmid=28316939 |pmc=5339638 |doi=10.5527/wjn.v6.i2.59 |url=}}</ref>
*Fludrocortisone: Use fludrocortisone 0.1 mg PO qd.
**'''2.5.1 [[Fludrocortisone]]:'''
**Reduce dose to 0.05 mg qd if transient hypertension develops.
***Preferred regimen (1): [[fludrocortisone]] 0.1 mg PO q24h.
**Maintenance dosage range: 0.1 mg 3 times weekly to 0.2 mg daily.  
****Reduce dose to 0.05 mg q24h if [[transient]] [[hypertension]] develops.
*Cortisone or hydrocortisone: Cortisone 10 to 37.5 mg q12h orally given in 2 divided doses with two-thirds of the total dose given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.)
****[[Maintenance dose|Maintenance dosage]] range: 0.1 mg 3 times weekly to 0.2 mg q24h.  
For complete therapy of adrenal insufficiency please [[Addison's disease medical therapy|click here.]]
**'''2.5.2 [[Cortisone]] or [[hydrocortisone]]:'''
***Preferred regimen (1): [[Cortisone]] 10 to 37.5 mg q12h [[Orally ingested|orally]] given in 2 divided doses with two-thirds of the total [[dose]] given in the morning (around 8 a.m.) and one third in the afternoon (noon to 4 p.m.).
For complete [[therapy]] in [[adrenal insufficiency]] please [[Addison's disease medical therapy|click here.]]


==References==
==References==
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Latest revision as of 15:29, 13 November 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2] Akshun Kalia M.B.B.S.[3]

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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