**3.3 Diagnosis of BKN**

*Perioperative Care for Organ Transplant Recipient*

delayed graft function and acute rejection. Other risk factors are male gender, older recipient age, diabetes, prolonged ureteral stent placement, smoldering subclinical graft inflammation, and/or abnormalities of dendritic cell and NK cell/T-cell activation. Relative over-immunosuppression by modern immunosuppressive drugs,

*Diagnosis of BK nephropathy: intranuclear viral inclusion bodies in tubular epithelial cells (A, HE, 200x), intracellular virions of 40–50 nm in diameter by electron microscopy (B, electron micrograph), intranuclear expression of SV-40 antigen in tubular epithelial cells (C) and/or epithelial cells of Bowman's capsule (D, both* 

Polyomavirus infection represents serological or virological evidence of virus exposure without distinguishing among replicating, latent, and transforming patterns. Manifest viral disease is, however, defined as histological evidence of polyomavirus-mediated organ pathology and is mainly limited to immunocompro-

though, is considered the main risk factor [47, 51, 54].

mised patients, such as transplant recipients [47, 55, 56].

**50**

**Figure 6.**

*SV-40, 400x).*

In order to confirm intrarenal BKV replication, renal biopsy remains the gold standard for a definitive diagnosis of BKN [51]. A minimum of two cores including the medulla are recommended to make a correct diagnosis, since in the early stage, viral inclusions may be present only in the medulla [5, 51, 57]. However, characteristic viral inclusion and tubular injury might be focally observed in the biopsy specimens, so PVN can be missed due to sampling error (**Figure 6**).
