Hypoaldosteronism medical therapy
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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]
- Prompt ECG must be obtained in all suspected patients of hypoaldosteronism as hyperkalemia may alter the 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.
- Drugs promoting hyperkalemia should be avoided, such as β blockers, ACE inhibitor, angiotensin receptor blockers and potassium-sparing diuretics.
- 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.
- Depending upon the volume status, patients may be treated with:
- In hypovolemic patients, 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.
Management of Hyperkalemia
- Calcium supplementation (calcium gluconate 10% (10ml), preferably through a central venous catheter as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias.
- 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.
- 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+ for Na+, thus leading to stimulation of the sodium-potassium ATPase.
- Salbutamol (albuterol, Ventolin®) is a β2-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 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 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®) 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.
Management on the basis of subtype of hypoaldosteronism
Hyporeninemic Hypoaldosteronism: Treatment is aimed at normalizing volume status, plasma potassium and aldosterone levels.[4][5][6]
- 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.
- Patients who cannot tolerate diuretics due to underlying hypotension or volume depletion are treated with:
- 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.
- Patients 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.
- 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 illness such as liver cirrhosis or heart failure.[7]
- 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.
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.[8]
Pseudohypoaldosteronism type I: Patients of pseudohypoaldosteronism are resistant to aldosterone or mineralocorticoid therapy and treatment is based on:[9]
- Correcting the underlying electrolyte abnormalities with sodium chloride (2 to 8 g/day) 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 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.
Primary or secondary adrenal insufficiency: These patients are treated with fludrocortisone and cortisol:[10]
- Fludrocortisone: Use fludrocortisone 0.1 mg PO qd.
- Reduce dose to 0.05 mg qd if transient hypertension develops.
- 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 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 click here.
References
- ↑ Magill SB (2014). "Pathophysiology, diagnosis, and treatment of mineralocorticoid disorders". Compr Physiol. 4 (3): 1083–119. doi:10.1002/cphy.c130042. PMID 24944031.
- ↑ Hrnciar J (1996). "[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]". Vnitr Lek (in Slovak). 42 (6): 394–9. PMID 8928409.
- ↑ Ettinger PO, Regan TJ, Oldewurtel HA (1974). "Hyperkalemia, cardiac conduction, and the electrocardiogram: a review". Am. Heart J. 88 (3): 360–71. PMID 4604546.
- ↑ 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.
- ↑ 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.
- ↑ Tan SY, Burton M (1981). "Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia". Arch. Intern. Med. 141 (1): 30–3. PMID 7004370.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.