Abstract: TH-PO165
Vedolizumab, a Monoclonal Antibody for Treating Crohn Disease, Can Cause T-Cell-Mediated Interstitial Nephritis and CKD
Session Information
- Drug Events Trainee Case Reports
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1800 Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
Authors
- Yin, Wenqing, Boston Medical Center, Boston, Massachusetts, United States
- Zhang, Ping L., William Beaumont Hospital, Royal Oak, Royal Oak, Michigan, United States
Introduction
Vedolizumab (Vedo), a gut-selective humanized monoclonal antibody, binds specifically to the α4 β7 integrin as a lymphocyte homing antagonist. Previously, Bailly et al have reported the first case of Veldo induced acute interstitial nephritis (AIN) (Am J Kid Dis 2017), with good renal recovery after the standard steroid treatment. Here, we report another case of Vedo associated AIN which resulted in CKD despite the standard steroid treatment. She was subsequently received steroid treatment without significant improvement of renal function (serum creatinine 1.8 mg/dl at the 3nd month follow-up following the biopsy). The case indicates that Vedo associated T cell medicated AIN can lead to a substantial CKD.
Case Description
A 33 years old woman with Crohn’s disease involving her small bowel and colon developed acute kidney injury with rising serum creatinine (from 0.7 to more than 2.0 mg/dl) after her receiving 3 standard doses of Vedo infusions over 2 months. Without signs of recovery after stopping the Vedo treatment, a renal biopsy was performed to evaluate her renal pathology. Light microscopy revealed AIN with only 10 % of B lymphocytes, 10% of CD8 positive macrophages, but 80% of T lymphocytes in the interstitium and mild tubulitis. Further stains showed 60% CD4 regulatory T lymphocytes and 40% of CD8 positive cytotoxic T lymphocytes. No eosinophils, neutrophils or granulomas were present. Kidney injury molecule-1 staining was positive in proximal tubules, consistent with an acute tubular injury secondary to AIN. Trichrome stained sections showed moderate interstitial fibrosis and tubular atrophy. Immunofluorescent studies and electron microscopy did not reveal additional specific findings.
Discussion
She has subsequently received steroid treatment without significant improvement of renal function (serum creatinine 1.8 mg/dl at the 3nd-month follow-up following the biopsy). The case indicates that Vedo associated T cell medicated AIN can lead to a substantial CKD.