Aldosterone (Aldo)

General Information

Primary hyperaldosteronism is caused by the overproduction of aldosterone by the cortex of the adrenal glands, (due to the presence of an adrenal adenoma or adrenal hyperplasia). The high aldosterone level increases the reabsorption of sodium and the loss of potassium by the kidneys, resulting in an electrolyte imbalance. Symptoms are not typically present, although muscle weakness can occur if potassium levels are very low.

The presence of hypokalaemia in a person with hypertension suggests the need to look for hyperaldosteronism.

Secondary hyperaldosteronism, which is more common, is a result of anything that increases renin levels, such as decreased blood flow to the kidneys, decreased blood pressure, or low sodium levels. The most important cause is narrowing of the blood vessels that supply the kidney, termed renal artery stenosis. Secondary hyperaldosteronism may also be seen with congestive heart failure, cirrhosis, kidney disease, and toxaemia of pregnancy.

Hypoaldosteronism (decreased production) usually occurs as part of adrenal insufficiency; it causes dehydration, low blood pressure, hyperkalaemia and hyponatraemia.

Patient Preparation

Ideally the laboratory should be provided with a full drug history and the patients sodium and potassium status. Advice with regard to drug therapy should be sought from the relevant Endocrinologist. The measurement of aldosterone is best carried out at 8 am following at least 4 hours recumbence. This is because the change in blood pressure upon standing causes release of renin and therefore an increase in aldosterone. In practice most samples for aldosterone are taken randomly.

Reference Range

Standing/random samples: <750pmol/L

Recumbent (minimum of 4 hours): <375pmol/L