Hyperaldosteronism describes an excess of the mineralocorticoid hormone aldosterone.
Patient with treatment-resistant hypertension and features of hypokalemia, such as muscle weakness, paraesthesia and constipation.
Primary hyperaldosteronism - excess aldosterone secondary to increased production from the zona glomerulus in the adrenal cortex, the glands act autonomously.
Conn’s syndrome - Another eponym; this refers to primary hyperaldosteronism caused by an aldosterone-producing adrenal adenoma.
Secondary hyperaldosteronism - excess aldosterone production due to increased activation of the RAAS system. The problem is not with the adrenal glands.
Patients may initially be asymptomatic and may be picked up on routine health checks with hypertension.
Polyuria (dilute urine), nocturia and polydipsia.
Hyperaldosteronism should be suspected in patients with treatment-resistant hypertension, especially if signs of hypokalaemia are present.
Both tests should show suppression of aldosterone production.
If high suspicion - i.e. biochemical evidence of hypokalemia, low plasma renin levels and high aldosterone levels; no confirmatory testing is required.
CT of the abdomen should be the initial Ix ordered to assess these patients.
Adrenal vein sampling should then be used to distinguish between unilateral/bilateral disease.
Ultrasound of the kidneys to assess for renal artery stenosis.
CT of the abdomen may be ordered to rule out a renin secreting tumour.
*aldosterone stimulates secretion of H+ via H+/ATPase in the intercalated cells of the collecting tubules.
Primary hyperaldosteronism in a patient aged <20 → test for familial hyperaldosteronism type I (also known as glucocorticoid remediable aldosteronism, GRA).
In very young patients → test for familial hyperaldosteronism type III (KCNJ5 mutation).
Unilateral disease (adenoma/hyperplasia) - laparoscopic adrenalectomy.
Bilateral disease (hyperplasia) – spironolactone 1st line, eplerenone is an alternative.
GRA - low dose glucocorticoid; aim is to suppress ACTH.*
*These patients have a mutation which increases the sensitivity of aldosterone synthase to ACTH.