What is the diagnosis and management for a patient with hyperaldosteronism and relatively normal plasma renin activity?

Diagnosis: Primary Aldosteronism with Unsuppressed Renin Due to Hypertensive Kidney Damage

Your patient has primary aldosteronism despite the relatively elevated plasma renin activity (PRA), likely due to secondary hypertensive kidney damage that has caused renin to "escape" from aldosterone-mediated suppression.

Understanding the Laboratory Values

Your aldosterone-to-renin ratio (ARR) calculation reveals the diagnosis:

• ARR = 17 ng/dL ÷ 15.07 ng/mL/h = 1.13 (This appears to be an error in your values as written)
• However, if aldosterone is 17 ng/dL and PRA is 1.507 ng/mL/h (decimal placement correction), then ARR = 11.3
• If PRA is truly 15.07, this represents markedly elevated renin that is paradoxical for primary aldosteronism 1

The key diagnostic insight: In severe, longstanding primary aldosteronism with hypertensive kidney damage, PRA can escape suppression while aldosterone remains inappropriately elevated for the sodium status 2. The disproportionately high aldosterone relative to clinical context (not absolute ARR cutoff) suggests autonomous aldosterone production 2.

Why Renin Is Not Suppressed

• Hypertensive nephrosclerosis from chronic aldosterone excess causes secondary activation of the renin-angiotensin system, overriding the volume expansion that normally suppresses renin 2
• This creates a "mixed picture" where both aldosterone and renin are elevated, but aldosterone remains inappropriately high for the degree of renin elevation 2
• Elevated serum creatinine often accompanies this presentation, indicating renal impairment 1

Confirmatory Testing Required

You must proceed with confirmatory testing despite the atypical ARR:

• Oral sodium loading test with 24-hour urine aldosterone measurement (failure to suppress aldosterone below threshold confirms autonomous production) 1
• Intravenous saline suppression test (2L normal saline over 4 hours; failure to suppress plasma aldosterone below 5 ng/dL confirms diagnosis) 1
• Ensure potassium repletion before testing, as hypokalemia suppresses aldosterone production 1
• Test with unrestricted salt intake and normal serum potassium 1

Subtype Determination

After biochemical confirmation:

• Non-contrast CT scan of adrenal glands as initial imaging 1
• Adrenal venous sampling (AVS) is mandatory before offering adrenalectomy to distinguish unilateral from bilateral disease 1
  • Up to 25% of patients would undergo unnecessary adrenalectomy based on CT findings alone 1
  • AVS is the gold standard for lateralization 1

Treatment Approach

For Unilateral Disease (Aldosterone-Producing Adenoma):

• Laparoscopic unilateral adrenalectomy is the treatment of choice 1, 3
• Improves blood pressure in virtually 100% of patients 1
• Cures hypertension in approximately 50% of cases 1
• Even with advanced hypertension and renal damage, patients benefit from adrenalectomy 2

For Bilateral Disease (Idiopathic Hyperaldosteronism):

• Spironolactone is first-line medical therapy 1, 3
  • Start at 100-400 mg daily for primary hyperaldosteronism 3
  • Titrate to lowest effective dose for long-term maintenance 3
• Eplerenone is an alternative with fewer anti-androgenic side effects 1

Critical Management Warnings

Monitor closely for hyperkalemia and worsening renal function when initiating spironolactone in patients with renal impairment:

• Patients with hypertensive kidney damage respond to spironolactone with marked increases in serum creatinine and potassium 2
• This occurs due to decreased filtered sodium load and mineralocorticoid receptor blockade 2
• Start with lower doses and monitor electrolytes and renal function closely 2
• Consider initiating therapy at 25 mg every other day if eGFR is 30-50 mL/min/1.73m² 3

Referral Recommendation

Refer immediately to a hypertension specialist or endocrinologist for all patients with confirmed primary aldosteronism 4, 1. This case is particularly complex given the unsuppressed renin and likely renal impairment, requiring subspecialty expertise for optimal management 1.

Key Clinical Pitfall to Avoid

Do not dismiss primary aldosteronism based on non-suppressed PRA alone 2. The traditional teaching that primary aldosteronism always presents with suppressed renin is incorrect in patients with severe hypertension and secondary kidney damage 2. The disproportionately elevated aldosterone relative to clinical context remains the diagnostic key 2.