Abstract: SA-PO1116
A Case of De Novo Fibrillary Glomerulonephritis in Post-Kidney Transplantation
Session Information
- Transplant Trainee Case Reports
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Tanjavour, Pooja, Newark Beth Israel Medical Center, Newark, New Jersey, United States
- De, Shreemayee, Newark Beth Israel Medical Center, Newark, New Jersey, United States
- Angeli, Daniel, Newark Beth Israel Medical Center, Newark, New Jersey, United States
- Adeboye, Adedamola M., Newark Beth Israel Medical Center, Newark, New Jersey, United States
- Lefkowitz, Heather Rush, The Nephrology Group PA, West Orange, New Jersey, United States
Introduction
Fibrillary glomerulonephritis (FGN) is a rare glomerular disease that results from deposition of Congo red-negative fibrils in glomerulus. Renal biopsy have shown that these fibrils, which consists of polymorphic IgG, are deposited mostly in mesangium and subendothelium areas. Recent studies show that DnaJ heat shock protein family member B9 (DNAJB9) has been associated with FGN. Patients usually present with nephrotic syndrome, hypertension, and hematuria. About 50% of the patients progress to end stage renal disease (ESRD). There are rarely reported cases of patients who present with de novo FGN post-kidney transplantation. Here we discuss a case of a patient with FGN post-kidney transplantation.
Case Description
This is a 61 year-old African American male with history of hypertension, ESRD on HD secondary to Diabetic Nephropathy, s/p Deceased Donor Renal transplant in March 2013, Hepatitis C, history of Banff 1A acute cell mediated rejection (August 2013), was evaluated for rise in creatinine to 3.1 from baseline of 2.0. in March 2019. He also had nephrotic-range proteinuria, hypertension without any other symptoms. He underwent transplant kidney biopsy, which showed Congo red-negative fibrillar deposits in glomeruli. Immunofluoroscence was consistent with FGN with lambda-chain restriction. He also had high Hepatitis C viral load of 273000 IU/ml. Immunofixation showed no monoclonal spike. FGN in this patient is presumed secondary to chronic Hepatitis C, thus was referred for Hepatitis C treatment and oncology referral for cancer screening.
Discussion
A retrospective study from University of North Carolina showed that among the FGN cases, Hepatitis C is most commonly reported in the African American population, and this is the group likely to transition to dialysis. Our patient was found to have high Hepatitis C viral load at the time of FGN diagnosis, thus supporting the hypothesis that Hepatitis C may be a causative factor of FGN. A case in 2013 reported a 56 year-old patient with a history of Hepatitis C who developed progressive renal graft failure due to FGN diagnosed 8 years after transplant. These studies indicate that Hepatitis C may be involved in developing fibrils in FGN, thus highlighting the importance of treating Hepatitis C virus for longer durability of renal allograft