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Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of the mineralocorticoid hormone aldosterone by the adrenal glands.[1] Aldosterone causes increase in sodium and water retention and potassium excretion in the kidneys, leading to arterial hypertension (high blood pressure). Also increase production of mineralocorticoid from the adrenal gland is evident. It is a rare but recognised cause of hypertension. The use of the term Conn’s syndrome should be restricted to adrenal adenoma, while primary aldosteronism can be due to other causes such as adrenal hyperplasia and adrenal carcinoma.
Primary hyperaldosteronism, aside from high blood pressure, may manifest with muscle cramps (due to hyperexcitability of neurons), muscle weakness (due to hypoexcitability of skeletal muscles), headaches (due to the low potassium or high blood pressure), and metabolic alkalosis (due to increased secretion of H+ ions by the kidney). The high pH of the blood makes calcium less available to the tissues and causes symptoms of hypocalcemia (low calcium levels).
It can be mimicked by liquorice ingestion (glycyrrhizin) and Liddle syndrome.
Measuring aldosterone alone is not considered adequate to diagnose primary hyperaldosteronism. Rather, both renin and aldosterone are measured, and the ratio is diagnostic.[2][3]
Usually, renin levels are suppressed, leading to a very low renin-aldosterone ratio (<0.0005). This test is confounded by antihypertensive drugs, which have to be stopped up to 6 weeks. If plasma levels of renin and aldosterone suggest hyperaldosteronism, CT scanning can confirm the presence of an adrenal adenoma. If the clinical presentation primarily involves hypertension and elevated levels of catecholamines, CT or MRI scanning can confirm a tumor on the adrenal medulla, typically a pheochromocytoma. The syndrome is due to:
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