Primary aldosteronism

Most common specifically treatable and potentially curable form of hypertension, accounting for at least 5% of hypertensive patients, with most patients being normokalaemic.

Approximately 30% have unilateral forms correctable by unilateral laparoscopic adrenalectomy, and 70% have bilateral forms in which hypertension responds well to aldosterone antagonist medicines.

Optimal detection involves screening all hypertensive patients using the plasma aldosterone/renin ratio, after controlling for factors (including medicines) that may confound results.

In patients with repeatedly elevated aldosterone/renin ratios, definitive confirmation or exclusion of diagnosis involves careful suppression testing with measurement of aldosterone response to fludrocortisone or to salt loading.

Subtype differentiation for optimal treatment involves genetic testing for the hybrid gene causing familial hyperaldosteronism type I (glucocorticoid-remediable aldosteronism). A negative genetic test should be followed by adrenal CT and adrenal venous sampling to differentiate unilateral from bilateral forms.

In primary aldosteronism (PA), aldosterone production exceeds the body's requirements and is relatively autonomous with regard to its normal chronic regulator, the renin-angiotensin II system.[1]Conn JW. Primary aldosteronism, a new clinical syndrome. J Lab Clin Med. 1955 Jan;45(1):6-17. http://www.ncbi.nlm.nih.gov/pubmed/13233623?tool=bestpractice.com [2]Conn JW. Plasma renin activity in primary aldosteronism. Importance in differential diagnosis and in research of essential hypertension. JAMA. 1964 Oct 19;190:222-5. http://www.ncbi.nlm.nih.gov/pubmed/14246593?tool=bestpractice.com This results in excessive sodium reabsorption via amiloride-sensitive epithelial sodium channels within the distal nephron, leading to hypertension and suppression of renin-angiotensin II. Urinary loss of potassium and hydrogen ions, exchanged for sodium at the distal nephron, may result in hypokalaemia and metabolic alkalosis if severe and prolonged.[1]Conn JW. Primary aldosteronism, a new clinical syndrome. J Lab Clin Med. 1955 Jan;45(1):6-17. http://www.ncbi.nlm.nih.gov/pubmed/13233623?tool=bestpractice.com [2]Conn JW. Plasma renin activity in primary aldosteronism. Importance in differential diagnosis and in research of essential hypertension. JAMA. 1964 Oct 19;190:222-5. http://www.ncbi.nlm.nih.gov/pubmed/14246593?tool=bestpractice.com