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Related Experiment Videos

BK Virus Nephropathy: Histological Evolution by Sequential Pathology.

B J Nankivell1, J Renthawa2, R N Sharma2

  • 1Department of Renal Medicine, Westmead Hospital, Westmead, Australia.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|April 4, 2017
PubMed
Summary
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BK virus allograft nephropathy (BKVAN) causes chronic kidney allograft infection and destruction. Early inflammation may mitigate injury, but high viral load predicts graft loss, highlighting the need for antiviral therapies.

Area of Science:

  • Nephrology
  • Virology
  • Transplant Immunology

Background:

  • BK virus reactivation in renal allografts leads to BK virus allograft nephropathy (BKVAN), a destructive chronic infection.
  • Understanding the histopathological evolution of BKVAN is crucial for managing kidney transplant outcomes.

Purpose of the Study:

  • To describe the sequential histopathological changes in BKVAN.
  • To identify factors predicting graft loss in BKVAN patients.
  • To characterize the role of inflammation and viral load in disease progression.

Main Methods:

  • Single-center retrospective cohort study of 63 kidneys from 61 patients with BKVAN.
  • Sequential histopathology analysis of 454 biopsies over a median follow-up of 60.1 months.
  • Comparison with time-matched control Banff scores from uninfected protocol biopsies.
Keywords:
clinical research/practicecomplication: infectiousinfection and infectious agentsinfectious diseasekidney transplantation/nephrologypathology/histopathologyviral: BK/JC/polyoma

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Main Results:

  • Interstitial inflammation occurred in 73% at diagnosis, correlating with viral histopathology and accelerating interstitial fibrosis and tubular atrophy (IF/TA).
  • Viral cytopathic effect led to subacute tubular injury, acute tubular necrosis, and IF/TA in 86.9% of cases.
  • High-level viremia, deceased donor status, and late acute rejection predicted graft loss; 38.1% of transplants failed.

Conclusions:

  • BKVAN is characterized by virus-induced tubular injury, inflammation, and progressive nephron destruction.
  • Cellular interstitial infiltration may mitigate subsequent tubular injury and viral load.
  • Effective antiviral therapy for BKVAN is a critical unmet clinical need.