Abstract: SA-PO273
Lupus Nephritis Due to Anti-TNF Alpha Therapy
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
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Nayyar, Kamal, NYU Winthrop Hospital, Mineola , New York, United States
- Santoriello, Dominick, Columbia University Medical Center, New York, New York, United States
- Drakakis, James, NYU Winthrop Hospital, Mineola , New York, United States
- Masani, Naveed N., NYU Winthrop Hospital, Mineola , New York, United States
Introduction
Drug induced lupus erythematosus is a lupus-like syndrome temporally related to continuous drug exposure which resolves upon drug discontinuation. Findings include skin manifestations, arthritis, serositis, and ANA/anti-DS DNA seropositivity. It can be divided into systemic, subacute cutaneous, and chronic cutaneous forms. Drugs most frequently associated are hydralazine, procainamide, and quinidine. In rare cases, anti-TNF alpha therapies have also been implicated. It is estimated that up to 10% of SLE cases are drug-induced. Such autoimmunity is idiosyncratic and unpredictable.
Case Description
An 80 year old male with a past medical history significant for DM II, hypertension, resolved hepatitis B infection, seropositive Rheumatoid Arthritis (RA), and CKD stage III with a baseline creatinine of 1.5 mg/dl was started on Etanercept (anti-TNF alpha therapy) due to severe erosive RA. After 6 months of treatment he presented with joint pains and swelling of the extremities, was noted to have acute renal failure with a creatinine of 2.0 mg/dl, proteinuria of 1.2 gm, new onset microscopic hematuria, hypocomplementemia, and anti -DsDNA/ANA seropositivity. Renal biopsy revealed diffuse endocapillary glomerulonephritis with immunofluorescence staining for IgG, IgA, C3, c1q, kappa and lambda; electron microscopy was devoid of tubuloreticular inclusion bodies. Given the lack of extra-renal SLE findings and the timing of etanercept, the biopsy findings were attributed to TNF-alpha inhibitor therapy, which was subsequently discontinued. The patient was treated with corticosteroids, with stabilization of renal parameters and resolution of anti-DsDNA and ANA positivity. Of note, the patient exhibited no other SLE type symptoms prior to or since TNF-alpha inhibitor therapy. Therapy for RA was switched to Rituximab.
Discussion
Anti-TNF alpha induced lupus represents a major therapeutic challenge. Most cases are caused by infliximab, followed by etanercept and adalimumab. Symptoms range from mild cutaneous lesions, to more systemic involvement including pericardial effusions, deep venous thrombosis, pneumonitis, and lupus nephritis. Most of the reported clinical features of anti-TNF-alpha -induced SLE present as cutaneous lesions, which are similar to those present in idiopathic SLE. This case exhibits the silent menace of the exceedingly rare anti-TNF-alpha induced lupus nephritis.