ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO1147

A Rare Case of JC Virus Nephropathy, Asymptomatic Progressive Multifocal Leukoencephalopathy, and Viremia in a Kidney Transplant Recipient

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Jayeola, Olakunle A., The University of New Mexico Department of Internal Medicine, Albuquerque, New Mexico, United States
  • Sosa, Nestor R., The University of New Mexico Department of Internal Medicine, Albuquerque, New Mexico, United States
  • Singh, Pooja P., The University of New Mexico Department of Internal Medicine, Albuquerque, New Mexico, United States
Introduction

Polyomavirus nephropathy (PVN) in kidney transplant recipients (KTR) is traditionally attributed to BK virus (BKV). JC virus-associated PVN is rare and likely underrecognized, particularly when routine BK testing is negative. The absence of well-defined management strategies further complicates this disease process in KTRs.

Case Description

A 78-year-old female s/p deceased-donor kidney transplant in January 2023, developed allograft dysfunction two years post-transplant (PT). Biopsy in December 2024 demonstrated focal SV40-positive staining consistent with polyomavirus nephropathy (PVN1), along with borderline T cell-mediated rejection treated with pulse-dose corticosteroids. Serial serum BK PCR remained undetectable, prompting JCV evaluation which revealed JC viremia and viruria. Brain MRI also showed periventricular white matter changes concerning for progressive multifocal leukoencephalopathy (PML). Cerebrospinal fluid PCR for JC virus was negative. Immunosuppression (IS) was continued at lower doses as no systemic symptoms were found, and intravenous immunoglobulin (IVIG) was initiated in February 2025, given at 1g/kg for two sequential doses every four weeks to date. AKI improved with corresponding decline in serum JCV from 1,900 copies/mL (April 2025) to an undetectable level (January 2026). The patient maintained a sustained virologic response without evidence of neurologic progression on physical examination or brain imaging.

Discussion

JCV-associated PVN is exceedingly rare and likely underrecognized due to the absence of routine surveillance. As SV40 staining does not distinguish polyomavirus species, PVN with negative BK viremia should prompt evaluation for JCV. Its dual tropism for renal tubular epithelium and central nervous system warrants neurologic evaluation given the high morbidity and mortality of PML. In the absence of neurological symptoms from PML, IVIG may offer a graft-preserving strategy with a sustained virologic response in JCV PVN.