Hypoaldosteronism medical therapy: Difference between revisions

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


==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|ACEi]], [[ARBs|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 [[Hypovolemia|hypovolemic]] [[patients]], [[Normal saline|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 [[Hypervolemia|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'''
* '''1.1 [[Calcium]] supplementation'''
** Preferred regimen (1): [[Calcium gluconate]] 10% (10ml)
*: '''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]]'''
** 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]].
* '''1.3 [[Bicarbonate]] therapy'''
** 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]].
* '''1.4  β<sub>2</sub>-selective agonist'''
** Preferred regimen (1): [[Salbutamol]] [[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.
* '''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 (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 (4): [[Patiromer]] [[anion]]
*: '''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 .


===Management of Hyperkalemia===
* '''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>
* [[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]].
** '''2.2.1:''' The primary focus of the treatment in hyperreninemic hypoaldosteronism is to treat the underlying condition.
* [[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]].
** '''2.2.2:''' Decreased level of [[aldosterone]] in patients of hyperreninemic hypoaldosteronism does not lead to any [[clinical]] [[complications]] and is therefore seldom treated.
* [[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]].
* [[Salbutamol]] ([[albuterol]], [[Ventolin]]<sup>®</sup>) is a β<sub>2</sub>-selective [[catecholamine]] that is administered by [[nebulizer]] (e.g. 10-20 mg).  This [[drug]] promotes movement of [[potassium]] into [[cells]], lowering the blood levels.
* [[Polystyrene sulfonate]] (Calcium Resonium, [[Kayexalate]]) is a binding resin that binds [[potassium]] within the [[Intestines|intestine]] and removes it from the [[body]] by [[defecation]]. Calcium Resonium (15g three times a day in water) can be given by [[mouth]]. [[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]].  This [[medication]] may cause [[diarrhea]].
* [[Refractory]] or severe cases may need [[dialysis]] to remove the [[potassium]] from the [[circulation]].
* 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]]).
* [[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.  


===Disease Name===
* '''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>
'''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>
** '''2.3.1 [[Aldosterone]] analogues:'''
*[[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 regime (1): 9α-[[fludrocortisone]] 0.05 to 0.2 mg q24h
*[[Patients]] who cannot tolerate [[diuretics]] due to underlying [[hypotension]] or [[volume depletion]] are treated with:
**: '''Note (1):''' Isolated hypoaldosteronism from [[CYP11B2]] [[gene]] [[mutation]] presents in [[infancy]] and are treated with 9α-[[fludrocortisone]].
**''[[Patients]] with normal [[renal function]]''[[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]].  
**: '''Note (2):''' In adults treatment is not necessary.<ref name="pmid26981183" />
**''[[Patients]] with [[Renal function impairment|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]].
*[[Aldosterone]] analogues are the third line therapy such as [[fludrocortisone]] in the dose of 0.1-0.3 mg/day.


'''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>  
* '''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>
* The primary focus of the treatment in hyperreninemic hypoaldosteronism is to treat the underlying condition.  
** Correcting the underlying [[electrolyte abnormalities]] with [[sodium chloride]] (2 to 8 g q24h) and cation-exchange resins such as [[sodium polystyrene sulfonate]].
* Decreased level of [[aldosterone]] in patients of hyperreninemic hypoaldosteronism does not lead to any [[clinical]] [[complications]] and is therefore seldom treated.
** [[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]].


'''Isolated Hypoaldosteronism''': Isolated Hypoaldosteronism from [[CYP11B2]] [[gene]] [[mutation]] presents in [[infancy]] and are treated with 9α-[[fludrocortisone]] 0.05 to 0.2 mg daily. 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>
* '''2.5 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>
 
**'''2.5.1 [[Fludrocortisone]]:'''
'''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>
***Preferred regimen (1): [[fludrocortisone]] 0.1 mg PO q24h.
* Correcting the underlying [[electrolyte abnormalities]] with [[sodium chloride]] (2 to 8 g/day) and cation-exchange resins such as [[sodium polystyrene sulfonate]].
****Reduce dose to 0.05 mg q24h if [[transient]] [[hypertension]] develops.
* [[Thiazide diuretics]] are used to treat [[hyperkalemia]]. In patients with severe [[hyperkalemia]] (>7.5 mmol/l) [[peritoneal dialysis]] may be done.
****[[Maintenance dose|Maintenance dosage]] range: 0.1 mg 3 times weekly to 0.2 mg q24h.  
* [[Pseudohypoaldosteronism]] decreases after few years and the [[therapy]] may be discontinued. However, these [[patients]] require [[salt]] supplementation till first 3-4 years of [[life]].
**'''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.).
'''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.
**Reduce dose to 0.05 mg qd if [[transient]] [[hypertension]] develops.
**[[Maintenance dose|Maintenance dosage]] range: 0.1 mg 3 times weekly to 0.2 mg daily.  
*[[Cortisone]] or [[hydrocortisone]]: [[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.]]
For complete [[therapy]] in [[adrenal insufficiency]] please [[Addison's disease medical therapy|click here.]]


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[[Category:Disease]]
[[Category:Endocrinology]]
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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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