Polyomavirus nephropathy: a brief review with special emphasis on clinico-patholgical aspects. 
From 1995 Polyomavirus (PyV) nephropathy (PVN) has played an important role in solid organ transplant recipients.  The disease is caused by a DNA virus, usually the BK variant, more rarely JC virus.  In immune incompetent patients either latent endogenous virus is reactivated, or donated virus can multiply.  The frequency of PVN nephropathy (previously 10% or higher) is declining.  The disease follows a stepwise course: viruria, viraemia, nephropathy.  Nephropathy usually manifests itself during the first year after transplantation.  The disease remains clinically silent for long periods, later progressive loss of renal function and renal failure occur.  A major risk factor is therapy with potent immune suppressive agents.  Morphologically, viral replication produces nuclear inclusions and necrosis, predominantly in the urothelium and tubular epithelium.  Inflammation (T and B lymphocytes, monocytes/macrophages and granulocytes) accompanies necrosis.  Progression is marked by tubular atrophy, interstitial fibrosis and transplant loss.  The virus can be detected by the electron microscope and, better, by immunohistology (preferentially mAb against SV40 Large T antigen).  It is often hard to differentiate PVN from an interstitial cellular rejection reaction (Banff 1 A/B).  As no effective drug treatment exists, the disease must be diagnosed as early as possible and immune suppression reduced.  Screening for polyomavirus reactivation is best done stepwise: search for urinary "Decoy cells" (PyV infected cells), PCR for PyV in the blood and in the case of reduced renal function, renal biopsy.  Compliance with a stringent screening algorithm allows early detection and adequate treatment and prevents organ loss.