Aldosterone and renin in systemic lupus erythematosus adore-sle study — ASN Events
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Aldosterone and renin in systemic lupus erythematosus adore-sle study (#372)

Chrislyn Ng 1 , Grace Feng 1 , Celine Shi 2 , Kathryn Connelly 2 3 , Laura E Eades 2 3 , Vera Golder 2 3 , Joanna Kent 4 , Emily Lin 2 3 , Kristy Yap 2 3 , Eric F Morand 2 3 , Alberta Y Hoi 2 3 , Jun Yang 1 5 6 , Fabien B Vincent 2
  1. Monash University, Melbourne, Victoria, Australia
  2. Centre for Inflammatory Diseases, School of Clinical Sciences at Monash Health, Melbourne, Victoria, Australia
  3. Department of Rheumatology, Monash Health, Melbourne, Victoria, Australia
  4. Department of Nephrology, Monash Health, Melbourne, Victoria, Australia
  5. Department of Endocrinology, Monash Health, Melbourne, Victoria, Australia
  6. Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Melbourne, Victoria, Australia

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease associated with a high burden of hypertension and cardiovascular disease. Primary aldosteronism (PA), a common but underdiagnosed cause of hypertension, may contribute to this burden. The Aldosterone and Renin in SLE (ADORE-SLE) study aims to prospectively assess the prevalence of PA in patients with SLE.

Adults with SLE attending Monash Health Lupus Clinic (Melbourne, Australia) were prospectively recruited from January 2021 to May 2025 and underwent PA screening with the plasma aldosterone-to-renin ratio (ARR). HTN was defined as systolic blood pressure (BP) ≥140mmHg and/or diastolic BP ≥90mmHg on at least two clinical visits, or a documented diagnosis of hypertension. Patients with elevated ARR (>70pmol/mU), suggestive of probable PA, were referred to the Endocrine Hypertension Clinic for further evaluation.

Among 73 participants recruited (median (IQR) age 51 (39-62) years; 89.8% female), ARR results were available for 59 (80.8%). At screening, 42 participants had established hypertension of whom 24 (40.7%) were receiving antihypertensive treatment, and another 18 (30.5%) had a new finding of elevated BP. An elevated ARR was observed in 5 patients, which represents 8.5% of the 59 patients with screening results or 11.9% of the 42 patients with concurrent SLE and hypertension. One participant completed saline suppression testing, establishing a diagnosis of PA, and achieved optimal BP control following initiation of spironolactone. An additional 12 participants (20.3%) were classified as having possible PA based on modified ARR/renin thresholds for those on interfering antihypertensive medications that typically cause false negative results.

PA may represent an under-recognised contributor to hypertension and cardiovascular risk in SLE. Preliminary findings from this study identified elevated ARR levels in at least 10% of SLE patients with hypertension, highlighting the need for larger studies and streamlined pathways integrating PA screening into rheumatology care to enable earlier diagnosis.