Abstract: SA-PO897
A Cascade of Viral Infection to Cardiomyopathy and Lupus Nephritis
Session Information
- Glomerular Diseases: Case Reports - 2
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Parkinson, William M., Brooke Army Medical Center, Fort Sam Houston, Texas, United States
- Wickham, Jesse M., Brooke Army Medical Center, Fort Sam Houston, Texas, United States
Introduction
Systemic Lupus Erythematosus (SLE) affects over 1.5 million Americans, causing significant morbidity and mortality. Lupus onset and flares can be triggered by a range of insults including medications, infections, and environmental factors. Lupus nephritis (LN) is a common manifestation of SLE with symptoms often including edema, hypertension or proteinuria. Lupus myocarditis highlights SLE cardiac involvement with heart failure symptoms. The wide spectrum of organ involvement with Lupus further complicates diagnosis. Appropriately phrased, Hickam’s dictum states, “A man can have as many diseases as he damn well pleases”. We present a case that highlights Hickam’s dictum with a tenuous presentation and multiorgan involvement.
Case Description
A 24-year-old active-duty female with a recent admission for pancreatitis presented to the emergency department with edema, fatigue, and found to be in cardiogenic shock. Previously, she was in excellent health, exercising, and fulfilling military requirements. Labs revealed proteinuria with dysmorphic red blood cells, elevated creatinine, ANA titer 1:320, and positive dsDNA. Kidney biopsy confirmed class III Lupus Nephritis. Cardiogenic shock was initially attributed to Lupus myocarditis. Cardiac MRI revealed an ejection fraction of 20%, dilated cardiomyopathy, severe valvular disease, but no myocarditis. Without myocarditis, Lupus is unlikely causative for cardiomyopathy. Further workup aimed at possible infectious etiologies revealing positive coxsackie antibody titers. The hospital course was further complicated by progressive biventricular failure requiring an intra-aortic balloon pump. Ultimately, the patient was stabilized and transferred for cardiac transplant evaluation. The presentation is thought to be a cascade of coxsackie virus infection driving both cardiomyopathy and new onset lupus with nephritis.
Discussion
The work up for complex patients requires a broad differential without bias. In this case, the initial concern was for Lupus induced myocarditis driving cardiogenic shock. However, further investigation revealed positive antibody titers for coxsackie virus and imaging not consistent with Lupus myocarditis. Broadening the differential to include infectious causes allowed the identification of prior coxsackie infection. This case highlights an interesting cascade from viral infection to cardiomyopathy and nephritis.