Abstract: SA-PO270
A Case of Golimumab-Associated Pauci-Immune Glomerulonephritis
Session Information
- Trainee Case Reports - VI
October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Wijayaratne, Sandhira, Harvard Medical School, Boston, Massachusetts, United States
- Agrawal, Nikhil, Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
- Kemp, Philip Scott, Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
- Kupferman, Joseph, Beth Israel Deaconess Medical Center, Brookline, Massachusetts, United States
Introduction
Golimumab is a monoclonal TNF-alpha inhibitor approved for rheumatoid arthritis (RA), ulcerative colitis (UC), psoriatic arthritis, and ankylosing spondylitis. It may be preferred in some patients due to easier dosing (monthly subQ injections) and ability to control symptoms in UC. Clinical trials studying golimumab have not reported glomerulonephritis as an adverse event, though there is at least one report of golimumab accelerating preexisting lupus nephritis. To our knowledge, there have been no reports of golimumab-associated, new-onset glomerulonephritis. Here, we present a patient with RA on golimumab who developed a pauci-immune crescentic glomerulonephritis with no signs of systemic vascultitis.
Case Description
87-year-old male with hypertension and rheumatoid arthritis referred by his rheumatologist with a creatinine of 2.6 mg/dL. He had a baseline creatinine of 1.29 mg/dL and 0.9 mg/dL, four months and nine months prior to his presentation, respectively. His RA was previously managed by steroids but was switched four years ago to monthly golimumab, last dose was 2 months ago. Urinalysis showed 3+ protein, negative leukocytes, 80-100 RBC/hpf, and 5-7 acanthocytes/hpf. Labs including C3, C4, ANA, ANCA, dsDNA, anti-histone antibody, cryoglobulin, Hepatitis B and C serologies, SPEP, UPEP were ordered; all eventually came back negative. Renal biopsy showed 18 of the 36 glomeruli had extracapillary proliferation, 14 of which had evidence of fibrinoid necrosis or cellular crescents. Findings were consistent with a diagnosis of pauci-immune crescentic glomerulonephritis. Over the course of the patient’s 5-day hospital stay, his creatinine was stable with a range of 2.5-2.8 mg/dL. He was discharged on 60 mg prednisone daily, golimumab was not restarted.
Discussion
This case represents the first report of crescentic pauci-immune glomerulonephritis associated with golimumab. With increasing use of TNF-alpha inhibitors, there lies a risk of increased episodes of glomerulonephritis associated with these medications. As with this patient, renal limited vasculitis may not appear until years into treatment, and could present with aggressive features. Patients should be monitored for glomerulonephritis and screening protocols with serial urinalysis and serum creatinine may be necessary. Long term data may help define relative risk with individual medications.