Hyperaldosteronism refers to excess aldosterone secretion. Excess aldosterone secretion may result from:
- a hypersecreting adrenal tumor of the aldosterone-secreting cells (Conn’s syndrome or primary hyperaldosteronism), or
- Inappropriately high activity of the renin-angiotensin system (secondary hyperaldosteronism)
Hyperaldosteronism can thus be either primary (as in when the adrenal cortex is secreting too much of the hormone on its own, without external influence) or secondary (as in when there is excessive stimulation of the adrenal cortex (zona glomerulosa) by angiotensin II.
Recall, angiotensin results from the activation of the renin-angiotensin-system.
CAUSES OF HYPERALDOSTERONISM
Primary hyperaldosteronism (Conn’s disease) is commonly caused by the presence of aldosterone-secreting tumor of the adrenal cortex. This tumor tends to produce aldosterone continually at a high, even in the absence of any form of stimulation. That is, this aldosterone-secreting tumor is autonomous.
The most common cause of primary hyperaldosteronism is tumor growth (adenoma) of the zona glomerulosa of the adrenal cortex.
Secondary hyperaldosteronism can result from any condition that causes prolonged reduction in arterial blood flow to the kidneys, thus, excessively activating the renin-angiotensin-aldosterone system. A classic example is atherosclerotic narrowing/stenosis of the renal arteries.
Primary hyperaldosteronism is however more common than the secondary form of this disease.
SYMPTOMS OF HYPERALDOSTERONISM
The symptoms of both primary and secondary hyperaldosteronism are traced to the exaggerated effects of aldosterone, namely;
- excessive Na+ retention (hypernatremia)
- K+ depletion (hypokalemia)
- increased fluid volume
- High blood pressure (hypertension)
High plasma levels of aldosterone stimulate Na+ reabsorption and potassium excretion in the distal tubule and collecting duct of the nephron. Consequently, patients develop hypernatremia with hypokalemia.
The excessive Na+ retention causes fluid retention as well which results in hypertension. This form of hypertension is difficult to treat by standard medications.
Because of the raised blood pressure and sodium (Na+) delivery to the macula densa (owing to increased filtered load of Na+), renin release is strongly inhibited. Thus, hyperaldosterone-induced hypertension is renin-independent and is one of the commonest causes of endocrine hypertension.