Cardiovascular · Year 1 · from Cardiovascular

Case 2: Primary Aldosteronism - Secondary Hypertension

Clinical Image

Source: Radiopaedia - Adrenal adenoma - Educational use

Patient Presentation

A 38-year-old woman is referred to endocrinology for evaluation of resistant hypertension. Despite taking three antihypertensive medications at maximum doses (including a diuretic), her blood pressure remains elevated. She has been experiencing muscle cramps, weakness, and fatigue. Her primary care physician noted that her potassium has been persistently low despite potassium supplementation.

Demographics

  • Age: 38 years
  • Sex: Female
  • Past Medical History: Hypertension diagnosed at age 32 (young-onset)
  • Medications: Amlodipine 10 mg, lisinopril 40 mg, chlorthalidone 25 mg, potassium chloride 40 mEq daily
  • Family History: No hypertension in immediate family

Chief Complaint

Resistant hypertension and recurrent hypokalemia despite supplementation

Physical Examination

  • Blood pressure: 168/102 mmHg (despite three medications)
  • Heart rate: 78 bpm
  • BMI: 26 kg/m2
  • General: Well-appearing
  • Cardiovascular: Normal S1/S2, no murmurs
  • Neurological: Proximal muscle weakness (difficulty rising from squat)
  • No cushingoid features, no abdominal bruit

Workup

  • Serum potassium: 2.9 mEq/L (low despite supplementation)
  • Serum sodium: 144 mEq/L (high-normal)
  • Plasma aldosterone concentration (PAC): 28 ng/dL (elevated)
  • Plasma renin activity (PRA): 0.2 ng/mL/hr (suppressed)
  • Aldosterone-to-renin ratio (ARR): 140 (elevated; >30 suggests primary aldosteronism)
  • Confirmatory test: Oral sodium loading - aldosterone remains elevated (not suppressed)
  • CT adrenal: 1.8 cm left adrenal adenoma, right adrenal normal
  • Adrenal vein sampling: Lateralizes to left adrenal gland

Diagnosis

Primary Aldosteronism (Conn Syndrome) due to Left Adrenal Aldosterone-Producing Adenoma

Treatment

  1. Hold interfering medications before testing (MRA, diuretics if possible)
  2. Preoperative preparation:
  • Spironolactone or eplerenone to control BP and correct hypokalemia
  • Potassium supplementation
  1. Laparoscopic left adrenalectomy (curative for unilateral adenoma)
  2. Postoperative monitoring:
  • BP typically normalizes or improves significantly
  • Monitor for transient hypoaldosteronism
  1. Long-term: If bilateral disease or surgery not pursued, medical therapy with mineralocorticoid receptor antagonist

Physiological Principles Demonstrated

  • Primary vs. secondary aldosteronism: In primary aldosteronism, the adrenal gland produces excess aldosterone autonomously. Renin is suppressed due to volume expansion and sodium retention. In secondary hyperaldosteronism (e.g., renal artery stenosis), renin is elevated.
  • Aldosterone effects: Aldosterone acts on the distal nephron to promote sodium reabsorption and potassium/hydrogen secretion. Excess aldosterone causes hypertension (volume expansion) and hypokalemia.
  • Resistant hypertension clues: Young onset, hypokalemia, and failure of multiple antihypertensives should raise suspicion for secondary causes.
  • Aldosterone-to-renin ratio: The ARR exploits the expected reciprocal relationship between aldosterone and renin to screen for autonomous aldosterone production.

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