When taking a blood test, the aldosterone-to-renin ratio is abnormally increased in primary<unk> , and decreased or normal but with high renin in secondary<unk> . 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). Primary Primary aldosteronism (hyporeninemic<unk>  was previously thought to be most commonly caused by an adrenal adenoma, termed Conn's syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases. Differentiating between the two is important, as this determines treatment. Also, see congenital adrenal hyperplasia. Adrenal carcinoma is an extremely rare cause of primary<unk> . Two familial forms have been identified: type I (dexamethasone suppressible), and type II, which has been linked to the 7p22 gene. 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<unk>  (also hyperreninism, or hyperreninemic<unk>  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<unk> . 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). Secondary<unk>  can also be caused by excessive ingestion of licorice or other members of the Glycyrrhiza genus of plants that contain the triterpenoid saponin glycoside known as glycyrrhizin. Licorice and closely related plants are perennial shrubs, the roots of which are used in medicine as well as making candies and in cooking other desserts because of the sweet taste. Through inhibition of 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), glycyrrhizin allows cortisol to activate mineralocorticoid receptors in the kidney. This severely potentiates mineralocorticoid receptor-mediated renal sodium reabsorbtion, due to much higher circulating concentrations of cortisol compared to aldosterone. This, in turn, expands the extracellular volume, increases total peripheral resistance and increases arterial blood pressure. The condition is termed pseudohyperaldosteronism. 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.
Hyperaldosteronism
Pseudohyperaldosteronism
Pseudohypoaldosteronism
Hypoaldosteronism
Familial hyperaldosteronism
Primary aldosteronism
Acromegaly
Apparent mineralocorticoid excess syndrome