Hyperaldosteronism

Question 1

Conn’s

Answer 1

Primary hyperaldosteronism

Question 2

Causes

Answer 2

bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases
adrenal adenoma: 20-30% of cases
unilateral hyperplasia
familial hyperaldosteronism
adrenal carcinoma

Question 3

Pathophysiology

Answer 3

aldosterone is high
renin is low (suppressed by volume expansion)
consequences:
aldosterone → ↑ renal tubular sodium resorption (via ENaC channels in the collecting duct)
↑ K⁺ excretion → hypokalaemia
↑ H⁺ excretion → metabolic alkalosis
hypertension from sodium/water retention

Question 4

Features

Answer 4

hypertension
increasingly recognised but still underdiagnosed cause of hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients, and is more common with adrenal adenomas
metabolic alkalosis

Question 5

Investigations

Answer 5

guidelines vary but certain patients should be screened for primary hyperaldosteronism, e.g.
hypertension with hypokalemia
treatment-resistant hypertension
the 2016 Endocrine Society recommend that a plasma aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism
should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
following this a high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
if the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia

Question 6

management

Answer 6

adrenal adenoma: surgery (laparoscopic adrenalectomy)
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone