The important points here are:
The important diagnostic indicators are:
Useful indicators are also a mild metabolic alkalosis (bicarbonate >30 mmols/l) and a mildly elevated serum glucose level due to the low potassium interfering with insulin secretion and glucose regulation. All tests should be made with the patient not taking any normal anti-hypertensive medication, such as diuretics and spironolactone, as this can invalidate the results.
Confirmatory findings are from blood tests showing:
Tests must be performed to indicate what the cause of the diagnosed primary hyperaldosteronism is as this determines the treatment.
CT or MRI scans of the adrenal glands will demonstrate any obvious tumours and indicate whether one or both glands are involved. They are sensitive enough to pick out more than 90% of APAs larger than 1 cm. If the mass is larger than 3 cm it is either an incidental finding unrelated to the hyperaldosteronism (an 'incidentaloma') or rarely a cancer secreting aldosterone. Imaging is less sensitive and specific for the remaining causes and any equivocal scan warrants further tests.
The principle here is that the adrenal adenomas producing aldosterone are sensitive to ACTH whereas bilateral idiopathic adrenal hyperplasia is sensitive to angiotensin II. Patients have blood tests at 08:00 for aldosterone, cortisol and renin after sleeping all night. After four hours of being upright and walking around (which stimulates angiotensin II production due to blood pressure changes, not affecting ACTH) the blood tests are repeated. Adrenal adenomas will show very little change in aldosterone levels whereas the benign adrenal hyperplasia cases will show increased aldosterone (due to stimulation by the increased angiotensin II.)
Diagram to illustrate posture studies - click to enlarge
This is an Angiotensin Converting-Enzyme (ACE) inhibitor (see physiology section) blocking angiotensin II production from angiotensin I. When given to patients with APA, plasma aldosterone levels remain unchanged due to the tumour being responsive only to ACTH. When given to patients with IHA, plasma aldosterone levels will fall as the hyperplastic glands are responsive to angiotensin II.
18-OHB is an intermediate compound produced in the synthesis of aldosterone from cholesterol in the adrenal cortex (see physiology section and section on Congenital Adrenal Hyperplasia). 18-OHF is formed from circulating cortisol in the adrenal cortex. Plasma and urine concentrations are elevated in most causes of primary hyperaldosteronism but are highest in glucocorticoid-suppressible aldosteronism (GSA), less high in APA and least high in IHA. This pattern can provide some useful information when used in conjunction with other tests.