MON-296 Tissue Sodium Content For Differential Diagnosis Of Essential Hypertension Versushyperaldosteronism: Baseline Characteristics Of The “See-Sodium-To-Treat (SSTT)” Trial

Abstract Disclosure: A. Marton: None. H. Tran: None. N. Morisawa: None. I.B. Osman: None. S. Saffari: None. R.S. Foo: None. P. Khong: None. T. Lim: None. A.M. Nagel: None. J. Titze: None. T. Puar: None. Introduction: Primary aldosteronism (PA) causes sodium retention and potassium loss. In the index patient described by Jerome Conn, a muscle biopsy performed during adrenalectomy demonstrated increased muscle sodium (Na+) and reduced muscle potassium (K+), reflecting physiological intracellular sodium and potassium derangements. Sodium (23Na)-MRI imaging is available to assess muscle Na+ content non-invasively. Methodology: Patients with suspicion of PA: hypertension and hypokalaemia, severe hypertension (blood pressure 150/100mmHg), resistant hypertension, young hypertension (age <40 years), and adrenal incidentaloma with hypertension are recruited from the Endocrinology outpatient clinics in Singapore. All patients undergo the standard PA diagnostic procedures including intravenous seated saline-loading test (SLT), and receive oral potassium supplementation to achieve serum K+ levels of 4mmol/L over 4-6 weeks prior to SLT. Eligible patients additionally attend 3 study visits: at baseline, after oral K supplementation but before the SLT (4-6 weeks) and after PA confirmation and treatment (6-12 months). During each study visit 23NaMRI imaging for muscle sodium quantification is performed and blood and 24h urine samples are collected for analysis. Plasma aldosterone concentration (PAC) and plasma renin activity (PRA) are measured by liquid-chromatography tandem mass spectrometry. Patients will be confirmed with PA if post-SLT PAC is 5ng/dL or greater with suppressed PRA (1ng/ml/hr or lower). The trial was approved by the SingHealth Centralised Institutional Review Board, Singapore, and was registered on ClinicalTrials.gov (NCT06569589). Results: We prospectively recruited 28 patients, with 15 females (53.6%), median age 51 years, and BMI of 26.6 kg/m2. At baseline visit 1, systolic blood pressure (BP) was 137.6±12.4 mmHg, diastolic BP 91.0±10.0 mmHg, and heart rate was 78.7 ±10.5 beats per minute. Plasma Na+ and K+ were 141.9±1.9 and 3.44±0.4 mmol/L; 24h Na+ and K+ excretion were 142.0±54.7 and 40.3±13.6 mmol/d. Baseline median PAC was 7.3 ng/dL (IQR: 3.3-10.3) and urinary aldosterone 4.8 μg/d (IQR: 2.7-6.6), and PRA was 0.88 ng/ml/hr (IQR: 0.4-2.2). Muscle Na+ content was 24.3 (IQR: 22.6-26.4) mmol/L tissue volume. Oral K+ supplementation instituted was 3.7±1.6 g/d prior to SLT. Summary and Conclusion: We will test the hypothesis that compared to patients diagnosed with essential hypertension, patients with hyperaldosteronism have a 10-20% higher muscle Na content (primary outcome 1). Secondary outcome measures are the effect of oral K+ supplementation, MR blockade, and surgical removal of aldosterone-producing adenoma on muscle Na+ content in the study participants. Presentation: Monday, July 14, 2025