Secreted by the adrenal cortex, aldosterone acts on the distal convoluted tube and causes reabsorption of sodium, potassium excretion and H + ions.
Its secretion is dependent on the renin-angiotensin system.
Its dosage is coupled to that of renin.
It is sometimes called “hormone of hypertension” and it is in this capacity that is measured.
Search primary aldosteronism suspected in hypertension, polyuria-polydipsia, muscle weakness access with hypokalemia.
Verify that the patient has followed the prescribed diet, normosodé enriched with potassium (3-4 g / d) for at least a week.
Collect urine for dosing control natriuresis (must be> 100 mEq / 24 h).
Ensure that the patient has stopped beta blockers for one week, diuretics, ACE inhibitors and NSAIDs for a fortnight, spironolactone for six weeks, as was prescribed.
Perform two samples of 5 mL of blood on heparin or EDTA:
• the first 8 am, lying on the patient from the night before (or at least for 1 h);
• the second after 1 h of walking.
Request the dosed aldosterone and plasma renin activity (PRA) in both samples.
• Subject lying (in normosodé scheme):
from 10 to 100 pg / mL (28-280 pmol / L)
• Subject standing (in normosodé scheme):
from 70 to 300 pg / ml (200 to 800 pmol / L)
• In cardiac failure, aldosterone can reach 3000 pg / ml (8322 pmol / L).
ng × 2.77 = pmol
pmol × 0.36 = ng
A decrease in aldosterone (with high renin) is observed in primary adrenal insufficiencies slow (Addison’s disease), where aldosterone is <10 pg / mL in the supine position.
Aldosterone is normal in the adrenal insufficiencies high pituitary origin.
Hypersecretion aldosterone causes:
• sodium reabsorption, which hypervolemia and hypertension;
• a potassium excretion, resulting in serum potassium <4 mEq / L with kaliuresis conserved (> 30 mmol / 24 h);
• a H + ion excretion hence alkalosis.
The diagnosis of aldosteronism suspected in cases of hypertension with hypokalemia is focused on the elevation of plasma aldosterone> 145 pg / mL contrasting with a collapsed renin activity, not stimulable (<5 pg / mL after 1 h of orthostatic).
Primary aldosteronism is due either to a unilateral adrenal adenoma (Conn syndrome) curable by surgery or hyperplasia of the two glands under medical treatment.
The distinction between adenoma and hyperplasia is difficult, by specialized services through dynamic tests and specific imaging tests.
Secondary hyperaldosteronism are far more numerous.
Most are due to hypersecretion of renin due to sodium depletion (diuretics) or hypovolemia (heart failure, ascites cirrhosis). Aldosterone is not measured in these situations.
Some rare, are due to decreased renal perfusion stenosis of the renal artery (dysplastic or atheromatous) increasing renin activity. They result in hypokalemia and hypertension with elevated aldosterone (3-5 times normal).
• aldosterone is low in chronic intoxications glycyrrhizin (excessive intake of licorice, pastis without alcohol) which causes, as Conn’s syndrome, hypertension with hypokalemia.
• Aldosterone remains normal in metabolic Hypercorticism (Cushing’s syndrome).