Abstract: PO2453
Polyomavirus Nephropathy with Crescent Formation
Session Information
- Transplant Complications: Infection
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1902 Transplantation: Clinical
Authors
- Binari, Laura, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Kapp, Meghan E., Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Schaefer, Heidi M., Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Concepcion, Beatrice P., Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction
Polyomavirus reactivation in an immunosuppressed transplant patient may cause polyomavirus nephropathy (PVN). Classically seen as a pleomorphic tubulointerstitial inflammatory reaction to the virally infected tubular epithelial cells, there are few reports of glomerular viral tropism. We present unique histopathologic findings of PVN including crescent formation with ultrastructural and immunohistochemical evidence of viral infection of glomerular epithelial cells in a kidney transplant recipient with acute kidney injury.
Case Description
A 52 y/o man s/p DDKT with well-controlled HIV presented with 2 weeks of worsening cough. He was diagnosed with multifocal pneumonia and disseminated CMV and VZV infection. His serum creatinine (SCr) and BK virus PCR were elevated to 3mg/dl (baseline 1.4-2.0 mg/dL) and 3.8M copy/mL respectively. He received ganciclovir and his immunosuppression was reduced. His pneumonia improved, but his BK PCR increased to 13.6M copy/mL and SCr remained elevated at 2.4 mg/dL.
A renal biopsy showed a diffuse plasma cell-rich pleomorphic interstitial inflammatory infiltrate, tubulitis, and acute tubular injury. Viral cytopathic effect was evident and an SV40 immunostain was positive in 60-70% tubular profiles, as well as parietal and visceral epithelial cells. EM revealed viral particles measuring 30 nm in diameter in tubular epithelial cells and a parietal epithelial cell. In addition, 7 of 21 total glomeruli had crescent formation with no GBM breaks or fibrinoid necrosis. There was no evidence of concomitant cellular or antibody-mediated rejection or CMV infection. These findings were indicative of PVN, with the rare finding of frequent crescents with glomerular epithelial cell infection.
Discussion
PVN is rarely described as having crescentic glomerular lesions, and if present, only one glomerulus per biopsy was affected. There are no reported cases of rapidly progressive glomerulonephritis in PVN. In our case, we found crescent formation more frequently in 33% of glomeruli. Additionally, viral cytopathic changes uncommonly affect glomeruli, typically only involving parietal epithelial cells when present. We demonstrated viral infection of both parietal and visceral epithelial cells. Our case highlights a pattern of kidney injury not commonly seen in PVN and supports that crescent formation can be caused by viral infection of the parietal epithelial cells.