PVAN occurs in 1–10% of renal transplant recipient during the first two years of transplantation. The disease is characterized by high level of BK virus replication in the renal tubular epithelial cells of the transplanted kidney leading to destruction of cells and epithelial denudation. This leads to tissue leakage and infiltration of inflammatory cells into the interstitium, ultimately leading to tubular atrophy and interstitial fibrosis. These changes cause reduction in graft function and graft loss.

Screening: This is recommended in all renal transplant recipients in every 3 months for first 2 years post-transplantation by quantitative PCR of urine or plasma.

 • BKPyV >7 log10 genome equivalent/mL in urine or >4 log10 genome equivalent/mL in plasma is considered significant.

• Because of intermittent shedding of BKPyV in urine, presence of virus in high concentration in plasma bears higher clinical significance.

• Presumptive diagnosis is made when the virus load in plasma is >4 log10 GEq/mL or VP1 mRNA >6.5 × 105 copies/ng of total RNA in urine.

Urinary findings: Presence of decoy cells and epithelial cells containing viral inclusions and urinary cast of polyomavirus aggregates.

Confirmative evidence: Features of renal histopathology provide the definitive evidence of BKPyVAN which are as follows:

• Intranuclear inclusions in tubular epithelial cells with enlarged nucleus and chromatin damage (Fig. 1a and b).

• Atrophy of tubules, interstitial fibrosis.

Fig1. a and b: Photomicrograph showing (a) pale eosinophilic (yellow arrow) and smudgy (red arrow) intranuclear inclusions of BK virus in distal tubular epithelial cell in a renal allograft biopsy (H&E, ×100 oil original magnification), (b) intranuclear inclusions (brown color) of BK virus in distal renal tubular epithelial cells by immunohistochemistry (×40 original magnification). (Photograph courtesy: Prof Ritambhra Nada, Department of Histopathology, PGIMER, Chandigarh.)

Summary of different clinical aspects of PVAN is depicted in Fig 2.

Fig2. Polyomavirus-associated nephropathy (PVAN)

Reduction or alteration of immunosuppressive therapy is the usual mode of treatment of PVAN and is effective in majority of cases. Other drugs like cidofovir, leflunomide or fluoroquinolone also have been tried in combination with reduction in immunosuppression, however, with no better result than reduction of immunosuppressive therapy alone.

Other diseases associated with BK virus:

 • Polyomavirus associated hemorrhagic cystitis: Mostly in patients with hematopoietic stem cell transplant (HSCT) recipients

• Ureteric stenosis

 • Central nervous system involvement

 • Interstitial pneumonia.

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مواضيع ذات صلة

Clinical Syndromes of Adenovirus

JCPyV and progressive multifocal leukoencephalopathy (PML)

Mechanisms of RNA virus genome replication

Epidemiology Human Papillomavirus

Pathogenesis of Human Papillomavirus

Clinical Syndromes of EBV

EBV Life Cycle

Epstein–Barr virus

Treatment of Cytomegalovirus

Diagnosis of Cytomegalovirus

Clinical Manifestations of Cytomegalovirus

The Viral Genome