Abstract: PUB034
Dysregulated Aldosterone Across the Spectrum of Hypertension: From New-Onset Hypertension to Advanced CKD with Resistant Hypertension
Session Information
Category: Cardiovascular-Kidney-Metabolic Health
- 602 Cardiovascular-Kidney-Metabolic Health: Clinical
Authors
- Singh, Amrinder, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States
- Patrick, Kennerly Clinton, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States
- Sriperumbuduri, Sriram, Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States
Introduction
Primary aldosteronism (PA) is classically associated with resistant hypertension and hypokalemia. However, aldosterone dysregulation may extend beyond these features and is often under-recognized, particularly in chronic kidney disease (CKD), where diagnostic uncertainty and therapeutic concerns limit evaluation.
Case Description
Case 1: A 50-year-old woman was found to have elevated blood pressures (~150/90 mmHg) on screening, with clinic values up to 154/115 mmHg. She had no hypokalemia or endocrine features. Renal function was normal. Plasma renin activity (PRA) was suppressed at 0.286 ng/ml/hr with plasma aldosterone of 9.4 ng/dL and serum potassium 3.9 mEq/L. A 24-hour urine collection demonstrated aldosterone excretion of 10.35 µg with adequate sodium intake. She was started on spironolactone 25 mg daily with improvement in blood pressure and biochemical parameters.
Case 2: A 54-year-old man with CKD stage 4 (eGFR 28 mL/min/1.73 m2, UACR 496 mg/g) and resistant hypertension on multidrug therapy had persistent blood pressures ~170/90 mmHg. Screening revealed PRA 0.683 ng/ml/hr and plasma aldosterone 23.3 ng/dL with serum potassium 4.5 mEq/L, consistent with inappropriate aldosterone activity. Spironolactone was initiated at 12.5 mg daily and titrated to 75 mg daily with clinical improvement. Further evaluation is ongoing.
Discussion
These cases highlight the broad spectrum of aldosterone dysregulation. The first demonstrates that aldosterone excess may be present in early hypertension without hypokalemia or traditional indications for screening. The second illustrates under-recognition in CKD, where concerns regarding interpretation and hyperkalemia often limit evaluation and use of mineralocorticoid receptor antagonists (MRAs).
Despite differing clinical contexts, both patients showed biochemical and clinical response to MRA therapy, supporting the presence of aldosterone-mediated disease. Current screening strategies, largely focused on classical phenotypes, may fail to identify such patients.
Conclusion: Aldosterone dysregulation spans a wide clinical spectrum and may be present in both early hypertension and advanced CKD. Absence of hypokalemia and presence of CKD should not preclude consideration of aldosterone excess.