Primary Aldosteronism in the Hospitalized Patient: Master the AHA/ACC Guidelines for Diagnosis and Organ-Sparing Management in the Acute Care Setting

In this episode of Hospital Medicine Unplugged, we break down hyperaldosteronism—recognize fast, test smart, and treat to protect the heart and kidneys.

We start with the big picture: primary aldosteronism (PA) drives up to 10% of hypertension cases, especially resistant hypertension, and carries outsized risks—atrial fibrillation, stroke, MI, CKD—even when BP looks controlled. Aldosterone excess wreaks havoc via sodium retention, potassium wasting, and vascular fibrosis.

When to screen? Think resistant hypertension, hypokalemia, adrenal incidentaloma, family history of early-onset HTN or stroke, and hypertension + OSA. Order PAC, PRA, and ARR (cutoff ARR ≥30 with PAC ≥10 ng/dL). Correct K⁺ first, keep salt intake normal, and stop MRAs 4 weeks prior if feasible. False negatives lurk if meds interfere—substitute with noninterfering agents (e.g., verapamil, hydralazine).

Confirmatory testing (saline infusion, oral sodium load, fludrocortisone suppression, or captopril challenge) seals the diagnosis. Then, differentiate subtype: CT for masses but remember, AVS is gold standard for surgical candidates, ensuring you don’t miss bilateral disease masquerading as unilateral.

Treatment tracks: • Unilateral disease → laparoscopic adrenalectomy. Expect cure or major BP improvement + normokalemia. Better CV/renal outcomes vs meds. • Bilateral disease or non-surgical → MRAs (spironolactone 12.5–25 mg → titrate; or eplerenone 25–50 mg BID if intolerant). Add salt restriction and other antihypertensives as needed.

Therapeutic goals: normalize BP with fewer meds, correct K⁺ without supplements, and see renin rise—your marker of effective blockade.

New horizons: aldosterone synthase inhibitors (e.g., lorundrostat) and ENaC blockers may expand the toolbox for those who can’t tolerate MRAs.

Monitoring matters: • Acute phase—check BP, K⁺, renal function daily; continuous ECG if severe hypokalemia. • After surgery—watch for hypoaldosteronism; track BP, K⁺, renin. • On MRAs—monitor for hyperkalemia, gynecomastia, renal decline; titrate carefully.

If left untreated? Expect refractory HTN, hypokalemic arrhythmias, LV hypertrophy, AF, strokes, MIs, and CKD progression—risks up to 4–12x higher for AF and 2–4x higher for CV events than essential hypertension.

Key takeaway: screen aggressively, confirm carefully, localize accurately, and treat decisively. Whether by scalpel or spironolactone, targeted therapy prevents irreversible cardiac and renal damage.