- Aldosteronism - excess secretion of aldosterone - can be:
- Primary - due to primary pathology of the adrenal gland
- Secondary - due to reduced plasma volume and increased angiotensin production
- Secondary aldosteronism is due to cirrhosis, nephrotic syndrome or cardiac failure
- Conn's syndrome is primary hyperaldosteronism due to:
- Aldosterone producing adenoma (50%)
- Bilateral idiopathic hyperplasia - idiopathic hyperaldosteronism (40%)
- Aldosterone secreting carcinoma
Pathophysiology
- Aldosterone is produced by the zona glomerulosa of the adrenal cortex
- Acts on distal convoluted tubule to increase sodium reabsorption
- Sodium reabsorption occurs at the expense of potassium and hydrogen ion loss
Picture provided by Dr Freddy Martinez, Hospital Juan Graham Casasus, Villahermosa, Tabasco,
Mexico
Clinical presentation
- Usually occurs between 30 and 60 years
- Conn's syndrome accounts for 1% of cases of hypertension
- Hypertension often responds poorly to treatment
- Biochemically there is usually a hypokalaemic alkalosis
- NB - serum potassium may be normal
Investigation
- Investigations need to:
- Confirm primary hyperaldosteronism
- Localise pathology
- If there is an adrenal mass is it producing aldosterone ?
- Diagnosis depend on demonstration of
- Reduced serum potassium:
- Increased urinary potassium excretion
- Increased plasma aldosterone
- CT is able to demonstrate 80% of adrenal adenomas
- MRI has a similar sensitivity
- Assessment of function may require isotope (NP59) scanning or renal vein sampling for aldosterone
Treatment
- If adrenal adenoma demonstrated - adrenalectomy is treatment of choice
- Requires preoperative spironolactone to increase serum potassium
- Blood pressure returns to normal in 70% of patients
- Hypertension associated with bilateral idiopathic hyperplasia is difficult to control
- Spironolactone alone or with an ACE inhibitor is often useful
Bibliography
Gleason
P T,
Weinberg M H,
Pratt J H et al.
Evaluation of diagnostic tests in the differential diagnosis of primary hyperaldosteronism.
J Urol 1993;
150:
1365-1368 |