Hyperaldosteronism - classification, etiology, pathogenesis, and clinical manifestations.
Hyperaldosteronism is a condition of excessive secretion of aldosterone, leading to sodium retention, hypertension, and hypokalemia.
Classification
- 1 Primary hyperaldosteronism (Conn syndrome)
Excess aldosterone production from adrenal glands independent of renin-angiotensin system.
- 2 Secondary hyperaldosteronism
Increased aldosterone secretion due to activation of renin-angiotensin system.
Etiology
Primary hyperaldosteronism
Aldosterone-producing adrenal adenoma (Conn syndrome) —most common.
Bilateral adrenal hyperplasia.
Adrenal carcinoma (rare).
Familial hyperaldosteronism (rare genetic forms).
Secondary hyperaldosteronism
Conditions causing increased renin production:
- Renal artery stenosis.
- Congestive heart failure.
- Cirrhosis with ascites.
- Nephrotic syndrome.
- Severe dehydration or diuretic use.
Pathogenesis
Primary hyperaldosteronism
- Autonomous excess aldosterone secretion → increased sodium and water reabsorption in distal renal tubules.
- Potassium and hydrogen ion excretion increased → hypokalemia, metabolic alkalosis.
- Sodium and water retention → hypertension, suppressed renin.
Secondary hyperaldosteronism
- Reduced renal perfusion or effective circulating volume → increased renin secretion.
- Renin stimulates angiotensin II → stimulates aldosterone secretion.
- Same downstream effects as primary form (sodium retention, potassium loss), but with high renin.
Clinical manifestations
Hypertension
Often moderate to severe.
Resistant to usual anti-hypertensive therapy.
Hypokalemia signs
Muscle weakness, fatigue.
Muscle cramps.
Paresthesias.
Possible arrhythmias.
Metabolic alkalosis
Due to hydrogen ion loss in urine.
Polyuria and polydipsia
Hypokalemia impairs renal concentrating ability → nephrogenic diabetes insipidus-like symptoms.
Specific clues
In primary hyperaldosteronism, renin is suppressed (low plasma renin activity).
In secondary hyperaldosteronism, renin is high.
Summary Table