Aldosterone is a steroid hormone produced by the zona glomerulosa of the adrenal cortex. It acts on the distal tubule and collecting ducts of the nephron to cause the conservation of sodium and secretion of potassium. Aldosterone increases reabsorption of sodium ions, and therefore water, increasing blood volume and blood pressure. Primary hyperaldosteronism (Conn's syndrome) may reflect increased aldosterone synthesis due to a benign adenoma in one of the adrenal glands or hyperplasia of both.
Hypertension with spontaneous or diuretic-induced hypokalaemia, especially in the presence of a sodium ≥140 mmol/L; Hypertension refractory to 3 or more drugs; Young hypertensives; Hypertension in presence of an incidental adrenal adenoma
|Less than six years = appropriate range will be given with the test results
Adult (random) = 90 – 700 pmol/L
Aldosterone to renin ratio used in clinical context to support/exclude diagnosis of primary hyperaldosteronism
Sample Required EDTA plasma preferred. Heparin (green top) or SST (gold top) also accepted
Sample Volume min 1 mL
The aldosterone:renin ratio is used in the clinical context to support/exclude diagnosis of primary hyperaldosteronism. For primary hyperaldosteronism, correct severe hypokalaemia (plasma potassium should be ≥ 3.0 mmol/L). Patients must be receiving an adequate intake of both sodium (100-150 mmol/24 h) and potassium (50-100 mmol/24 h) and discontinue the supplementation temporarily for 24 hours before blood samples are taken. All interfering drugs should be discontinued if at all possible for a minimum of 2 weeks (aldosterone antagonists for 6 weeks). If not possible, antihypertensive drugs may be continued for an initital screening sample with the exception of spironolactone and oestrogen (stop for at least 4 weeks), β-blockers and NSAIDs (stop for at least 1 week).