Abstract: TH-PO703
Apixaban-Induced IgA Vasculitis with Nephritis
Session Information
- Glomerular Diseases: Case Reports - 1
October 24, 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
- Jatoi, Tahir Ahmed, SUNY Downstate Health Sciences University, New York City, New York, United States
- Sasidharan, Sandeep Raja, SUNY Downstate Health Sciences University, New York City, New York, United States
- Akram, Rabiya, SUNY Downstate Health Sciences University, New York City, New York, United States
- Abushawer, Mohammad Waleed, VA New York Harbor Healthcare System, New York, New York, United States
- Pariya, Fnu, SUNY Downstate Health Sciences University, New York City, New York, United States
- Amjad, Arfa, SUNY Downstate Health Sciences University, New York City, New York, United States
- Saggi, Subodh J., SUNY Downstate Health Sciences University, New York City, New York, United States
- Grossman, Susan, VA New York Harbor Healthcare System, New York, New York, United States
- Michel, Marie-Alex, VA New York Harbor Healthcare System, New York, New York, United States
- Salifu, Moro O., SUNY Downstate Health Sciences University, New York City, New York, United States
Introduction
Leukocytoclastic vasculitis (LCV), previously called Henoch-Schönlein purpura, is characterized by IgA-dominant immune deposits affecting small vessels and often involves the skin, gastrointestinal tract, joints, and kidneys. Direct oral anticoagulants are an emerging cause of LCV. This is a diagnosis of exclusion. In cases of drug-induced LCV, discontinuation of offending agent is the mainstay of treatment. Steroids may have a role in treating cases with widespread skin involvement. We are presenting a rare case of Apixaban induced leukocytoclastic vasculitis (LCV) with Nephritis
Case Description
71 y.o. male with PMH of CKD3b, DM, CAD, COPD, HTN, LE DVT with B/L bilateral leg swelling for 6 months, admitted with c/o extensive pruritic rash after being started on Apixaban for 2 weeks. Vital signs and system review were otherwise unremarkable. On PE, he had open skin lesions with draining clear fluid and LE swelling. Labs showed BUN/Creat of 54/2.1, from baseline of 1.6, HGB 11 mg/dl, UA had proteinuria with significant microhematuria, Upcr of 3.7 g/g from 0.5 g/g, IgE levels were elevated 1020, rest of the nephrotic work up was negative. Skin biopsy revealed leukocytoclastic vasculitis. Due to worsening creatinine and proteinuria, renal biopsy was performed, and it showed globally sclerotic glomeruli with moderate interstitial fibrosis and tubular atrophy on light microscopy, IgA staining positive on immunofluorescence with dense deposits in mesangium on electron microscopy. The patient was switched from apixaban to warfarin, and started on prednisone and Mycophenolate Mofetil with a diagnosis of IgA vasculitis and nephritis. Renal function and proteinuria improved.
Discussion
Apixaban is a rare cause of leukocytoclastic vasculitis (LCV). To our knowledge, there are only a few reported cases of LCV due to apixaban in the literature. Our case is the only case of apixaban associated LCV with Nephritis. LCV is a diagnosis of exclusion after infectious, autoimmune, and inflammatory conditions have been excluded. Almost 30% of all cases of LCV are drug-induced. However, anticoagulants are a rare cause of LCV. Our case of apixaban-induced LCV with nephritis highlights a rare complication of a common medication, which is important for physicians to be aware of.