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Primary aldosteronism (PA), also known as primary hyperaldosteronism, refers to the excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels and high blood pressure. [1] This abnormality is a paraneoplastic syndrome (i.e. caused by hyperplasia or tumors).
Primary aldosteronism (hyporeninemic hyperaldosteronism) is most often caused by bilateral idiopathic (micronodular) adrenal hyperplasia (almost 70% of cases) [4] and adrenal adenoma (Conn's syndrome) (about 30% of cases). [4] These cause hyperplasia of aldosterone-producing cells of the adrenal cortex resulting in primary hyperaldosteronism.
Glucocorticoid remediable aldosteronism also describable as aldosterone synthase hyperactivity, is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient. It is a cause of primary hyperaldosteronism. [1]
In physiology, aldosterone escape is a term that has been used to refer to two distinct phenomena involving aldosterone that are exactly opposite each other: . Escape from the sodium-retaining effects of excess aldosterone (or other mineralocorticoids) in primary hyperaldosteronism, manifested by volume and/or pressure natriuresis.
Spironolactone, the first member of the class, is also used in the management of hyperaldosteronism (including Conn's syndrome) and female hirsutism (due to additional antiandrogen actions). Most antimineralocorticoids, including spironolactone, are steroidal spirolactones. Finerenone is a nonsteroidal antimineralocorticoid.
Secondary hyperaldosteronism, on the other hand, is due to overactivity of the renin–angiotensin system. Conn's syndrome is primary hyperaldosteronism caused by an aldosterone-producing adenoma. Depending on cause and other factors, hyperaldosteronism can be treated by surgery and/or medically, such as by aldosterone antagonists.
Hyperaldosteronism is caused by the adrenal gland's overproduction of the hormone aldosterone. The excess production of the adrenal gland, specifically the zona glomerulosa, is the cause of primary hyperaldosteronism. Excessive renin-angiotensin-aldosterone system activation results in secondary hyperaldosteronism. [29]
The cutoff normal individuals from those with primary hyperaldosteronism is significantly affected by the conditions of testing, such as posture and time of day. On average, an ARR cutoff of 23.6 ng/dL per ng/(mL·h), expressed in alternative units as 651 pmol/L per μg/(L·h), has been estimated to have a sensitivity of 97% and specificity of 94%. [2]