Hyperaldosteronism
Hyperaldosteronism | |
---|---|
Other names | Aldosteronism[1] |
Aldosterone | |
Specialty | Endocrinology |
Symptoms | Nocturia |
Hyperaldosteronism is a
This cause of mineralocorticoid excess is primary hyperaldosteronism reflecting excess production of aldosterone by adrenal zona glomerulosa. Bilateral micronodular hyperplasia is more common than unilateral adrenal adenoma.
Signs and symptoms
It can be asymptomatic, but these symptoms may be present:[2]
- Fatigue
- Headache
- High blood pressure
- Hypokalemia
- Hypernatraemia
- Hypomagnesemia
- Intermittent or temporary paralysis
- Muscle spasms
- Muscle weakness
- Numbness
- Polyuria
- Polydipsia
- Tingling
- Metabolic alkalosis[3]
- Nocturia
- Blurry Vision
- Dizziness/Vertigo
Cause
The causes of primary hyperaldosteronism are
Diagnosis
When taking a
Types
In endocrinology, the terms 'primary' and 'secondary' are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, i.e., the tumor's location. It also refers to causes that are genetic (primary) or due to another condition or influence (secondary).[citation needed]
Primary
Primary aldosteronism (hyporeninemic hyperaldosteronism) was previously thought to be most commonly caused by an
Two familial forms have been identified: type I (dexamethasone suppressible), and type II, which has been linked to the 7p22 gene.[6]
Features
- Hypertension
- Hypokalemia (e.g., may cause muscle weakness)
- Alkalosis
Investigations
- High serum aldosterone
- Low serum renin
- High-resolution CT abdomen
Management
- Adrenal adenoma: surgery
- Bilateral adrenocortical hyperplasia: aldosterone antagonist, e.g., spironolactone
Secondary
- Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).
Secondary refers to an abnormality that indirectly results in pathology through a predictable physiologic pathway, i.e., a renin-producing tumor leads to increased aldosterone, as the body's aldosterone production is normally regulated by renin levels. One cause is a juxtaglomerular cell tumor. Another is renal artery stenosis, in which the reduced blood supply across the juxtaglomerular apparatus stimulates the production of renin. Likewise, fibromuscular dysplasia may cause stenosis of the renal artery, and therefore secondary hyperaldosteronism. Other causes can come from the tubules: low reabsorption of sodium (as seen in Bartter and Gitelman syndromes) will lead to hypovolemia/hypotension, which will activate the renin–angiotensin system (RAAS).[7]
Secondary hyperaldosteronism can also be caused by excessive ingestion of
Secondary hyperaldosterone can also be caused by a genetic mutation in the kidneys which causes sodium and potassium wasting. These conditions can be referred to syndromes such as Bartter Syndrome and Gitelman Syndrome.[9]
Treatment
Treatment includes removing the causative agent (such as licorice), a high-potassium, low-sodium diet (for primary) and high-sodium diet (for secondary),
Other animals
Cats can be affected by hyperaldosteronism. The most common signs in cats are muscle weakness and loss of eyesight, although only one of these signs may be present.[11] Muscle weakness is due to low potassium concentrations in the blood, and signs of muscle weakness, such as being unable to jump, may be intermittent.[11] High blood pressure causes either detachment of the retina, or blood inside the eye, which leads to loss of vision.[11] Hyperaldosteronism caused by a tumor is treated by surgical removal of the affected adrenal gland.[11]
See also
References
- ^ "aldosteronism" at Dorland's Medical Dictionary
- ^ "Hyperaldosteronism". The Lecturio Medical Concept Library. Retrieved 23 July 2021.
- ^ "Hyperaldosteronism: eMedicine Pediatrics: General Medicine". Retrieved 2009-06-16.
- PMID 6029811.
- ^ "Hyperaldosteronism". The Lecturio Medical Concept Library. Retrieved 25 July 2021.
- PMID 11073536.
- PMID 29763159. Retrieved 23 July 2021.
- S2CID 207495149.
- PMID 21503667.
- PMID 24857581.
- ^ PMID 32653266.