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Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
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).
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]
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.
The difference between primary hyperaldosteronism and secondary hyperaldosteronism lies in the causation of excess aldosterone, where primary hyperaldosteronism refers to the overproduction of aldosterone from the adrenal glands, and secondary hyperaldosteronism refers to the overactivation of the RAAS system.
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]
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]
Hyponatremia (due to hypoaldosteronism) - Aldosterone is the end product of the renin-angiotensin-aldosterone system that regulates blood pressure via blood pressure surveillance in the Kidney Juxtaglomerular apparatus. Aldosterone normally functions to increase sodium retention (which brings water as well) in exchange for potassium.