Human Polyoma Virus-Associated Interstitial Nephritis in the Allograft Kidney1

Abstract

Polyoma virus tubulo-interstitial nephritis-associated graft dysfunction usually calls for judicious decrease in immunosuppression and monitoring for acute rejection. Development of methods to serially quantify the viral load in individual patients could potentially improve clinical outcome.

Polyomavirus Allograft Nephropathy: Sequential Assessment of Histologic Viral Load, Tubulitis, and Graft Function Following Changes in Immunosuppression

“…The diagnosis was confirmed in all cases by immunohistochemistry or in-situ hybridization, as previously reported (2). Viral infection localized to the nuclei in the tubular epithelium.…”

“…Polyomavirus nephropathy (PVAN) is an increasingly recognized complication in kidney transplant recipients (1)(2)(3)(4)(5). The histology is characterized by viral inclusions, interstitial inflammation, and tubulitis.…”

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

“…The re-emergence of polyomavirus allograft nephropathy (PVAN) has been amply documented in many centers (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). The specific factors that influence outcome are not known, but graft loss has been attributed to a late diagnosis of PVAN in kidneys already showing irreversible tissue damage (scarring) (7).…”

Detection and expression of human BK virus sequences in neoplastic prostate tissues

“…It persistently infects almost 100% of the human population by early childhood (Gardner, 1973;Padgett, 1981;Do¨rries et al, 1994). It resides in the kidneys in a latent or persistent state, but can be reactivated upon immunosuppression of the host and is associated with hemorrhagic cystitis and polyomavirus nephropathy (Arthur et al, 1986;Hiraoka et al, 1991;Pappo et al, 1996;Randhawa et al, 1999;Li et al, 2002). BKV oncogenically transforms rodent cells in culture, causes kidney tumors in transgenic mice, and transforms primary human cells in culture when coexpressed with an activated ras oncogene (Portolani et al, 1975;Pater and Pater, 1986;Small et al, 1986;Dalrymple and Beemon, 1990).…”