Latent and productive polyomavirus infections of renal allografts: morphological, clinical, and pathophysiological aspects.

Polyomavirus allograft nephropathy, also termed BK virus nephropathy (BKN) after the main causative agent, the polyoma-BK-virus strain, is a major complication following kidney transplantation. BKN is the most common viral infection affecting the renal allograft with a reported prevalence of 1% up to 10%. It often leads to chronic allograft dysfunction and graft loss. BKN is most likely caused by the reactivation of latent BK viruses which, under sustained and intensive immunosuppression, enter a replicative/productive cycle. Viral disease, i.e., BKN, is typically limited to the kidney transplant. It is histologically defined by the presence of intranuclear viral inclusion bodies in epithelial cells and severe tubular injury. Virally induced tubular damage is the morphological correlate for allograft dysfunction. In this chapter, different variants of polyomavirus intranuclear inclusion bodies [types 1 through 4] and adjunct techniques [immunohistochemistry, in-situ hybridization, electron microscopy and polymerase chain reaction (PCR)] that are used for proper characterization of disease are described. Special emphasis is placed on the clinical and pathophysiological significance of different histological stages of BKN.