Secondary Hypertension: Primary Aldosteronism (PA)
Secondary Hypertension: Primary Aldosteronism (PA)
Source : Medscape , September 08, 2025, based on ESC 2025 & Current Evidence
1. Prevalence & Importance
• PA is now the most common cause of secondary endocrine hypertension.
• Occurs in ~10–20% of all hypertensives and up to 40% of resistant HTN.
• Often underdiagnosed because of limited screening.
2. Pathophysiology
• Autonomous aldosterone secretion → sodium retention, potassium & H⁺ loss.
• Results in HTN, hypokalemia, metabolic alkalosis.
• CV risk is higher than essential HTN, even at same BP.
3. Clinical Clues
• Resistant or severe HTN.
• HTN + hypokalemia (spontaneous or diuretic-induced).
• Adrenal incidentaloma.
• Early-onset HTN or family history of early stroke.
4. Screening (Step 1)
• Aldosterone–Renin Ratio (ARR) = preferred initial test.
High aldosterone + suppressed renin = suggestive.
• Confirmatory testing is required in borderline biochemical results that are still in favor of abnormal.
• Options: Saline infusion test, Oral sodium loading, Fludrocortisone suppression, Captopril challenge.
6. Subtype Classification (Step 3)
• Imaging (CT/MRI) for adrenal mass.
• Adrenal venous sampling (AVS): Do it in inconclusive imaging (small nodules, mild asymmetry); can skip if clear unilateral adenoma and strong biochemistry.
7. Main Etiologies
• Bilateral idiopathic hyperplasia (most common).
• Aldosterone-producing adenoma (Conn’s).
• Rare: familial forms (types 1–5), carcinoma, ectopic secretion.
8. Treatment
• Unilateral (adenoma) → laparoscopic adrenalectomy (curative in many).
• Bilateral hyperplasia → medical therapy (mineralocorticoid receptor antagonists: spironolactone, eplerenone; ± amiloride).
• Familial GRA → glucocorticoids + standard therapy.
9. Prognosis
• Without treatment: ↑ risk of stroke, MI, arrhythmias, LVH, kidney damage.
• Proper surgery or targeted medical therapy → markedly reduces CV risk.
