Endocrine hypertension

Clinical information

Endocrine hypertension makes up around 10% of all hypertension cases. The most frequent causes of endocrine hypertension are primary hyperaldosteronism, Cushing's syndrome and pheochromocytoma. Other causes include hyperthyroidism, primary hyperparathyroidism and acromegaly.

Primary hyperaldosteronism (Conn's syndrome) is characterised by an increased aldosterone concentration and renin suppression. The hormone aldosterone is produced from cholesterol in the adrenal cortex. It is a mineralocorticoid and is regulated via the renin-angiotensin-aldosterone system (RAAS). The protease renin is formed in the juxtaglomerular cells of the kidney and secreted into the blood. As part of the RAAS it breaks up the glycoprotein angiotensinogen to form angiotensin I (Ang I). Ang I is processed into Ang II via the angiotensin-converting enzyme (ACE). Ang II, in turn, stimulates the production of the hormone aldosterone. Aldosterone acts mainly in the kidneys, increasing the resorption of sodium from the distal tubules and the excretion of potassium. The resulting rise in the potassium level increases the blood volume and blood pressure.

Secondary hyperaldosteronism is much rarer than the primary form. It is the result of an overstimulation of the RAAS and is thus characterised by increased aldosterone and renin levels. 

Diagnostics

In suspected cases of hyperaldosteronism, the guidelines by the Endocrine Society recommend determining the aldosterone and renin concentrations and calculating the aldosterone-renin ratio (ARR).

Files

Chemiluminescence immunoassays: aldosterone and direct renin measurement