Abstract: PUB569
Pauci-Immune Crescentic Glomerulonephritis with Re-Initiation of Adalimumab for Crohn Disease
Session Information
Category: Trainee Case Report
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Hartley, Robert C., University of Utah, Salt Lake City, Utah, United States
- Gilligan, Sarah, University of Utah, Salt Lake City, Utah, United States
- Ramkumar, Nirupama, University of Utah, Salt Lake City, Utah, United States
- Westenfelder, Christof, University of Utah, Salt Lake City, Utah, United States
- Al-Rabadi, Laith, University of Utah, Salt Lake City, Utah, United States
- Gregory, Martin C., University of Utah, Salt Lake City, Utah, United States
- Agarwal, Adhish, University of Utah, Salt Lake City, Utah, United States
- Revelo Penafiel, Monica Patricia, University of Utah, Salt Lake City, Utah, United States
- Abraham, Josephine, University of Utah, Salt Lake City, Utah, United States
Introduction
Inflammatory bowel disease (IBD) is associated with a number of renal disease processes most commonly nephrolithiasis, IgA nephropathy and interstitial nephritis. Certain tumor necrosis factor alpha (TNFa) inhibitors, which are commonly used for treatment of IBD, have been rarely associated with pauci immune crescentic glomerulonephritis (PICG). We present a unique case of PICG in the setting of re-initiation of adalimumab (TNFa inhibitor) in a patient with Crohn’s disease (CD)
Case Description
A 40-year-old woman presented with CD flare and abdominal pain, nausea, vomiting, poor oral intake, an intermittent pruritic rash and gross hematuria. She was treated with a steroid taper and re-initiation of adalimumab. On initial evaluation she was hypertensive with diffuse abdominal pain. Laboratory evaluation was notable for a serum creatinine for 3.6 mg/dL up from a baseline for 0.8 mg/dL, hematuria and proteinuria of 6.6 g/g. Serologic studies including ANA, MPO, PR3, hepatitis B and C and anti-GBM were negative. Complement C3 and C4 were normal. Imaging showed perinephric stranding and a small non-obstructing stone. Patient was treated with steroids, adalimumab, and IV fluids. Serum creatinine peaked at 5.8 mg/dL and then trended down and patient was discharged home with close renal follow up. She was readmitted with recurrent abdominal symptoms and a worsening serum creatinine and underwent a renal biopsy six weeks after initial evidence of acute kidney injury. Pathology showed PICG. She was treated with rituximab and an intensified steroid regimen. For her CD, she was transitioned from adalimumab to vedolizumab (an oral monoclonal antibody with gut selective anti-inflammatory activity) due to concern that adalimumab contributed to her PICG. At last follow up her serum creatinine was down trending but had not returned to normal.
Discussion
The TNFa inhibitors infliximab and etanercept have a rare association with PICG and in renal biopsy case series of patients with a history of IBD PICG has been reported. However, the association of adalimumab with ANCA negative PICG in this case is unique in the literature and may represent an under recognized etiology of glomerulonephritis in IBD.