Primary Aldosteronism (PA), as defined by the autonomous and inappropriate secretion of aldosterone, causes mineralocorticoid hypertension. Key features of this include suppression of plasma renin and hypokalaemia. Recent studies that have used the ratio of aldosterone to renin (ARR) as a screening test have suggested that the prevalence of PA in unselected populations of patients with hypertension is around 10%. Only a minority of these patients, however, have a low potassium level.
More detailed evaluation of patients thought to have PA on the basis of a raised ARR is appropriate. It is important to note that some antihypertensive drugs can affect the ratio. For example, betablocker therapy reduces renin and is associated with an increased risk of false positive results when the ARR is used as a screening test. Ideally, therefore, drug therapy should be withdrawn when patients are being investigated. A variety of suppression tests are recommended thereafter, the most simple of which is to re-measure the aldosterone to renin ratio in patients during oral sodium loading.
When autonomous aldosterone production is identified, search for a lateralising adenoma is appropriate. This will require a combination of imaging and, where necessary, adrenal vein sampling for aldosterone. The true prevalence of solitary aldosterone producing adenomas in this circumstance remains a matter of debate, particularly as a substantial number of patients with apparent lateralising lesions have evidence of histological change affecting the rest of their renal zona glomerulosa, suggesting that Primary Aldosteronism forms part of a more generalized abnormality of adrenal mineralocorticoid synthesis.
In subjects where aldosterone secretion cannot be shown to lateralise, a search for other rare causes of aldosterone excess, including glucocorticoid remedial aldosteronism, is appropriate.
03 - 05 Nov 2003
Society for Endocrinology