Diagnostic challenges in primary aldosteronism evaluation and finerenone use.
Primary aldosteronism (PA) is a common but frequently ignored cause of hypertension, particularly in patients with normal serum potassium and aldosterone levels.
We report the case of a 70-year-old Han Chinese man with a 20-year history of hypertension who presented with normokalemia and normal plasma aldosterone levels. Despite this, laboratory evaluation revealed suppressed direct renin concentration (DRC) and a markedly elevated aldosterone-to-renin ratio (ARR), raising suspicion for PA. Adrenal computed tomography demonstrated bilateral nodular adrenal thickening. The patient had persistently uncontrolled blood pressure despite triple antihypertensive therapy with amlodipine besylate, valsartan/hydrochlorothiazide, and bisoprolol. Spironolactone was added to the existing regimen but was subsequently discontinued due to intolerance. Treatment was then switched to finerenone, a nonsteroidal mineralocorticoid receptor antagonist. During follow-up, blood pressure was well controlled, serum potassium levels remained stable, and both plasma renin concentration and the aldosterone-to-renin ratio normalized.
This case highlights the diagnostic challenge of PA evaluation in a patient with normal-range aldosterone and suppressed renin and provides clinical experience with finerenone after intolerance to a steroidal mineralocorticoid receptor antagonist.
We report the case of a 70-year-old Han Chinese man with a 20-year history of hypertension who presented with normokalemia and normal plasma aldosterone levels. Despite this, laboratory evaluation revealed suppressed direct renin concentration (DRC) and a markedly elevated aldosterone-to-renin ratio (ARR), raising suspicion for PA. Adrenal computed tomography demonstrated bilateral nodular adrenal thickening. The patient had persistently uncontrolled blood pressure despite triple antihypertensive therapy with amlodipine besylate, valsartan/hydrochlorothiazide, and bisoprolol. Spironolactone was added to the existing regimen but was subsequently discontinued due to intolerance. Treatment was then switched to finerenone, a nonsteroidal mineralocorticoid receptor antagonist. During follow-up, blood pressure was well controlled, serum potassium levels remained stable, and both plasma renin concentration and the aldosterone-to-renin ratio normalized.
This case highlights the diagnostic challenge of PA evaluation in a patient with normal-range aldosterone and suppressed renin and provides clinical experience with finerenone after intolerance to a steroidal mineralocorticoid receptor antagonist.