Abstract: PUB285
Early Lupus Nephritis (LN) Unmasked by Refractory Hypertension (HTN) and Pericarditis in Systemic Lupus Erythematosus (SLE)
Session Information
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Channagiri, Ritu, Florida Atlantic University Charles E Schmidt College of Medicine, Boca Raton, Florida, United States
- Richards, Marc, Florida Atlantic University Charles E Schmidt College of Medicine, Boca Raton, Florida, United States
Introduction
SLE is a complex autoimmune disease with multisystem involvement. Serositis, resistant HTN, and proteinuria may signal subtle, progressive LN. We present a 23-year-old male athlete with no prior medical history who developed lupus pericarditis followed by refractory HTN and urinary abnormalities concerning for evolving LN. He presented with pleuritic chest pain, palpitations, syncope, and dyspnea.
Case Description
Imaging revealed moderate pericardial and pleural effusions; pericardial drainage was performed. Echocardiography showed a small persistent pericardial effusion without hemodynamic compromise. Labs revealed ANA 1:640, dsDNA IgG 139 IU/mL, and C4 6 mg/dL. He was diagnosed with SLE and started on corticosteroids, later transitioned to azathioprine and belimumab. Symptoms improved, though serologies remained elevated. He was maintained on prednisone 10 mg daily. Months later, he developed HTN refractory to amlodipine 10 mg, clonidine 0.2 mg, eplerenone 50 mg, and olmesartan 20 mg. Eplerenone was increased to 100 mg and chlorthalidone 25 mg added, but HTN persisted. He also developed ocular inflammation. Urinalysis revealed 0.6 g/day proteinuria, 10 RBCs and WBCs/hpf, and serum albumin 3.0 g/dL. eGFR remained >60 mL/min/1.73m^2. Serial urinalyses showed intermittent 2+ proteinuria, 2+ hematuria, 1+ urobilinogen, and up to 19 WBCs/hpf. These findings raised concern for early LN, with biopsy results pending for confirmation.
Discussion
This case highlights the complexity of evolving LN and the need to recognize early signs. While initial symptoms responded to immunosuppression, persistent serologic activity and new urinary findings suggested renal involvement. Proteinuria, hematuria, and leukocyturia without infection are hallmark features and may precede overt nephritic or nephrotic syndrome. Resistant HTN may reflect early glomerular dysfunction, with impaired sodium handling and endothelial injury contributing to volume overload. In suspected proliferative LN, switching from azathioprine to mycophenolate mofetil is often favored. Though not standard in SLE, IL-1 inhibitors may help in refractory serositis when steroids and NSAIDs are limited. Timely biopsy and treatment adjustment are key to preserving renal function. Emerging therapies may support steroid-sparing approaches for glomerular and extraglomerular lupus manifestations.