Hypoaldosteronism natural history, complications and prognosis: Difference between revisions
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==Overview== | ==Overview== | ||
If left untreated, hypoaldosteronism | If left untreated, hypoaldosteronism leads to [[hyperkalemia]] which can alter the function of [[Electrical conduction system of the heart|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 gland|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== | ==Natural History, Complications, and Prognosis== | ||
===Natural History=== | ===Natural History=== | ||
*If left untreated, hypoaldosteronism can progress to hyperkalemia and hyponatremia with | *If left untreated, hypoaldosteronism can progress to [[hyperkalemia]] and [[hyponatremia]] with [[hypovolemia]] or [[hypervolemia, complications and prognosis|hypervolemia]].<ref name="pmid18053465">{{cite journal |vauthors=Sood MM, Sood AR, Richardson R |title=Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia |journal=Mayo Clin. Proc. |volume=82 |issue=12 |pages=1553–61 |year=2007 |pmid=18053465 |doi=10.1016/S0025-6196(11)61102-6 |url=}}</ref><ref name="pmid6268928">{{cite journal |vauthors=Sterns RH, Cox M, Feig PU, Singer I |title=Internal potassium balance and the control of the plasma potassium concentration |journal=Medicine (Baltimore) |volume=60 |issue=5 |pages=339–54 |year=1981 |pmid=6268928 |doi= |url=}}</ref><ref name="pmid15786818">{{cite journal |vauthors=Mann JF, Yi QL, Sleight P, Dagenais GR, Gerstein HC, Lonn EM, Bosch J |title=Serum potassium, cardiovascular risk, and effects of an ACE inhibitor: results of the HOPE study |journal=Clin. Nephrol. |volume=63 |issue=3 |pages=181–7 |year=2005 |pmid=15786818 |doi= |url=}}</ref> | ||
*Hyperkalemia is an acute life threatening condition since it can alter the electrical activity of the heart and lead to life threatening | *[[Hyperkalemia]] is an acute life threatening condition since it can alter the [[Electrical conduction system of the heart|electrical activity of the heart]] and lead to life threatening [[arrhythmias]]. | ||
*Patients with severe hyperkalemia (>7.5 mmol/l) may present with [[Bundle branch block|bundle branch blocks]] or [[Fascicular block|fascicular blocks]]. | *Patients with severe [[hyperkalemia]] (>7.5 mmol/l) may present with [[Bundle branch block|bundle branch blocks]] or [[Fascicular block|fascicular blocks]]. | ||
*When serum [[potassium]] level ≥ 9 mEq/L, hyperkalemia may lead to [[ventricular fibrillation]], [[PEA]] and even [[cardiac arrest]]. | *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. | *[[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 | *[[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 [[Hypervolemia|hypervolemic]]. | ||
===Complications=== | ===Complications=== | ||
*Common complications of hypoaldosteronism include: | *Common [[complications]] of hypoaldosteronism include:<ref name="SousaCabral2016">{{cite journal|last1=Sousa|first1=André Gustavo P|last2=Cabral|first2=João Victor de Sousa|last3=El-Feghaly|first3=William Batah|last4=Sousa|first4=Luísa Silva de|last5=Nunes|first5=Adriana Bezerra|title=Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management|journal=World Journal of Diabetes|volume=7|issue=5|year=2016|pages=101|issn=1948-9358|doi=10.4239/wjd.v7.i5.101}}</ref> | ||
**Hyperkalemia | **[[Hyperkalemia]] | ||
**Hypotension | **[[Hypotension]] | ||
**Hypovolemia | **[[Hypovolemia]] | ||
**Metabolic acidosis | **[[Metabolic acidosis]] | ||
**Hyponatremia | **[[Hyponatremia]] | ||
===Prognosis=== | ===Prognosis=== | ||
*Depending on the extent of the hyperkalemia and underlying renal or adrenal condition at the time of diagnosis, the prognosis of hypoaldosteronism may vary. | *Depending on the extent of the [[hyperkalemia]] and underlying [[renal]] or [[adrenal]] condition at the time of [[diagnosis]], the [[prognosis]] of hypoaldosteronism may vary.<ref name="SousaCabral2016">{{cite journal|last1=Sousa|first1=André Gustavo P|last2=Cabral|first2=João Victor de Sousa|last3=El-Feghaly|first3=William Batah|last4=Sousa|first4=Luísa Silva de|last5=Nunes|first5=Adriana Bezerra|title=Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management|journal=World Journal of Diabetes|volume=7|issue=5|year=2016|pages=101|issn=1948-9358|doi=10.4239/wjd.v7.i5.101}}</ref><ref name="pmid12133029">{{cite journal |vauthors=Ahmed A |title=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? |journal=J Am Geriatr Soc |volume=50 |issue=7 |pages=1297–300 |year=2002 |pmid=12133029 |doi= |url=}}</ref><ref name="pmid15017529">{{cite journal |vauthors=Mangrum AJ, Bakris GL |title=Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in chronic renal disease: safety issues |journal=Semin. Nephrol. |volume=24 |issue=2 |pages=168–75 |year=2004 |pmid=15017529 |doi= |url=}}</ref> | ||
*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. | *[[Prognosis]] is generally good for patients of hypoaldosteronism who receive treatment. | ||
*Patient having underlying renal insufficiency or diabetic nephropathy generally progresses to end stage stage renal disease. Drugs such as | *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 renal disease|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== | ==References== | ||
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Latest revision as of 16:39, 18 October 2017
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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
Natural History
- 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.
Complications
- Common complications of hypoaldosteronism include:[4]
Prognosis
- 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.