A 38-year-old woman presents to the clinic with a 6-month history of progressive headaches and occasional palpitations. Her blood pressure is 168/112 mmHg bilaterally. Physical examination reveals a regular pulse of 98 bpm, no abdominal bruits, and normal fundoscopy. Serum electrolytes are normal (K⁺ 4.2 mEq/L), and renal function is preserved (creatinine 0.9 mg/dL). Plasma renin activity is suppressed at 0.3 ng/mL/hr (normal 0.5–1.5). A 24-hour urine aldosterone is elevated at 18 μg (normal < 12 μg). What is the most likely diagnosis?

Explanation

## Clinical Presentation & Key Findings **Key Point:** The combination of hypertension, suppressed plasma renin activity (PRA), and elevated 24-hour urine aldosterone is pathognomonic for primary hyperaldosteronism (Conn syndrome). ## Diagnostic Reasoning ### The Aldosterone-Renin Axis In primary hyperaldosteronism: 1. Autonomous aldosterone secretion → sodium retention → volume expansion 2. Volume expansion suppresses renin release → **low PRA** 3. Elevated aldosterone despite suppressed renin = **inverted aldosterone-to-renin ratio** | Feature | Primary Hyperaldosteronism | Secondary Hyperaldosteronism | Essential HTN | |---------|----------------------------|------------------------------|---------------| | **Plasma Renin Activity** | Suppressed (< 1 ng/mL/hr) | Elevated | Normal to elevated | | **24-hr Urine Aldosterone** | Elevated (> 12 μg) | Elevated | Normal | | **Aldosterone-to-Renin Ratio** | > 30 | < 10 | < 10 | | **Serum K⁺** | Low (often < 3.5) | Normal or low | Normal | | **Metabolic Alkalosis** | Common | Possible | Absent | **High-Yield:** The suppressed renin is the critical differentiator. In secondary causes (renovascular disease, diuretic use), renin is elevated because the kidney senses volume depletion or reduced perfusion pressure. ### Why This Patient Has Primary Hyperaldosteronism - **Suppressed PRA (0.3)** rules out secondary causes - **Elevated aldosterone (18 μg)** confirms autonomous production - **Normal K⁺** suggests mild/early disease or genetic variant (familial hyperaldosteronism type I) - **No abdominal bruit** makes renovascular disease unlikely - **Young female** — typical demographic for Conn syndrome ## Next Steps in Diagnosis 1. **Confirmatory test:** Saline suppression test (aldosterone should suppress < 5 ng/dL after 4 L normal saline IV) 2. **Subtype differentiation:** CT adrenal imaging ± adrenal vein sampling (to distinguish aldosterone-producing adenoma vs. bilateral idiopathic hyperplasia) **Clinical Pearl:** Hypokalemia is absent in ~30% of cases, especially if diagnosed early or if the patient has concurrent use of potassium-sparing agents. Do not exclude Conn syndrome based on normal K⁺ alone. **Mnemonic — RAAS Axis in HTN:** **SEAR** = Suppressed renin, Elevated Aldosterone, Autonomous production, Renovascular disease ruled out. [cite:Harrison 21e Ch 297]