Hypoaldosteronism natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

If left untreated, hypoaldosteronism leads to hyperkalemia which can alter the function of cardiac conduction pathways. Depending upon the severity of hypoaldosteronism, hyperkalemia can be a life threatening condition. When serum potassium rises above ≥ 9 mEq/L, hyperkalemia may lead to ventricular fibrillation, PEA and even cardiac arrest. Common complications of hypoaldosteronism include hyperkalemia, metabolic acidosis, hypotension, hypovolemia and hyponatremia. Depending on the extent of the hyperkalemia and underlying renal or adrenal condition at the time of diagnosis, the prognosis of hypoaldosteronism may vary. Prognosis of hypoaldosteronism is generally good for patients who receive treatment.

Natural History, Complications, and Prognosis

If left untreated, hypoaldosteronism can progress to hyperkalemia and hyponatremia with hypovolemia or hypervolemia.^[1]^[2]^[3]
Hyperkalemia is an acute life threatening condition since it can alter the electrical activity of the heart and lead to life threatening arrhythmias.
Patients with severe hyperkalemia (>7.5 mmol/l) may present with bundle branch blocks or fascicular blocks.
When serum potassium level ≥ 9 mEq/L, hyperkalemia may lead to ventricular fibrillation, PEA and even cardiac arrest.
Hyponatremia is unusual in isolated hypoaldosteronism since under normal conditions cortisol leads to suppression of ADH. However, patients of adrenal insufficiency have decreased cortisol and aldosterone which may progress to hyponatremia.
Aldosterone deficiency leads to decreased sodium and water absorption which predisposes to hypovolemia. However, patients with underlying conditions such as kidney disease or heart condition may be hypervolemic.

Depending on the extent of the hyperkalemia and underlying renal or adrenal condition at the time of diagnosis, the prognosis of hypoaldosteronism may vary.^[4]^[5]^[6]

Prognosis is generally good for patients of hypoaldosteronism who receive treatment.
Untreated patients risk having hyperkalemia which is associated with cardiac arrhythmias that can be fatal.
Patient having underlying renal insufficiency or diabetic nephropathy generally progresses to end stage stage renal disease. Drugs such as ACE inhibitor and angiotensin receptor blockers which are the mainstay of treatment with diabetes and renal dysfunction are avoided in hypoaldosteronism since these may lead to hyperkalemia.

References

↑ Sood MM, Sood AR, Richardson R (2007). “Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia”. Mayo Clin. Proc. 82 (12): 1553–61. doi:10.1016/S0025-6196(11)61102-6. PMID 18053465.
↑ Sterns RH, Cox M, Feig PU, Singer I (1981). “Internal potassium balance and the control of the plasma potassium concentration”. Medicine (Baltimore). 60 (5): 339–54. PMID 6268928.
↑ Mann JF, Yi QL, Sleight P, Dagenais GR, Gerstein HC, Lonn EM, Bosch J (2005). “Serum potassium, cardiovascular risk, and effects of an ACE inhibitor: results of the HOPE study”. Clin. Nephrol. 63 (3): 181–7. PMID 15786818.
↑ ^4.0 ^4.1 Sousa, André Gustavo P; Cabral, João Victor de Sousa; El-Feghaly, William Batah; Sousa, Luísa Silva de; Nunes, Adriana Bezerra (2016). “Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management”. World Journal of Diabetes. 7 (5): 101. doi:10.4239/wjd.v7.i5.101. ISSN 1948-9358.
↑ Ahmed A (2002). “Use of angiotensin-converting enzyme inhibitors in patients with heart failure and renal insufficiency: how concerned should we be by the rise in serum creatinine?”. J Am Geriatr Soc. 50 (7): 1297–300. PMID 12133029.
↑ Mangrum AJ, Bakris GL (2004). “Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in chronic renal disease: safety issues”. Semin. Nephrol. 24 (2): 168–75. PMID 15017529.

Overview