Hypoaldosteronism medical therapy

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Hypoaldosteronism Microchapters

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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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