Kidney nontumor
Infections / parasites
BK virus / polyomavirus

Author: Nikhil Sangle, M.D. (see Authors page)

Revised: 21 March 2018, last major update September 2012

Copyright: (c) 2003-2018, PathologyOutlines.com, Inc.

PubMed Search: BK virus polyomavirus [title] kidney pathology

Cite this page: Sangle, N. BK virus / polyomavirus. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/kidneybkvirus.html. Accessed July 21st, 2018.
Definition / general
  • Polyomaviruses are nonenveloped DNA viruses, 45 nm in diameter; members of papovavirus family, which also contain papillomavirus
  • Polyomavirus BK is widely present in healthy individuals, but latent in kidneys, central nervous system and B cells
  • Other polyoma viruses are JC (causes progressive multifocal leukencephalopathy) and SV40 (causes subclinical infections)
  • JC and BK virus infection is very prevalent in the first 2 years after kidney transplant (J Res Med Sci 2011;16:916)
  • Immunosuppression promotes reactivation of latent polyoma virus, leading to viral replication in renal tubular epithelial cells
Clinical features
  • BKV strain of polyoma virus may cause renal failure in AIDS patients, is reactivated in < 8% of renal transplant patients with heavy immunosuppression or rarely in other immunosuppressed patients
  • Rarely occurs in nonrenal solid organ transplantation (Am J Transplant 2010;10:2324)
  • Diagnose by PCR (but variant strains may affect quantitation of viral load, J Clin Microbiol 2011;49:4072); urinary decoy cell detection (Transplantation 2011;92:1018) and immunostains (SV40 immunostain crossreacts with JCV)
  • Increased risk with ureteral stenting (Transplant Proc 2011;43:2641)
  • Associated with interstitial nephritis, infection of glomerular epithelial cells and crescents (minority of cases)
  • JC virus strain of polyoma virus usually not associated with renal damage (Hum Pathol 2001;32:656), but present in renal tissue in 6% of AIDS patients (Mod Pathol 2003;16:35)
Case reports
Microscopic (histologic) description
    In non transplanted kidney:
  • Interstitial inflammation, atrophic tubules with large and eosinophilic nuclei

    In allograft kidney:
  • Viral cytopathic effect with large, homogenous and purple intranuclear inclusions, primarily in tubular epithelium (Hum Pathol 2004;35:367)
  • No necrosis (as seen in HSV), no perinuclear halo (as seen in CMV)
  • Also ischemic glomerulopathy (62%), aneurysmal dilation of glomerular capillaries (28%) and mild increase in mesangial matrix (23%)
  • Viral cytopathic effect in parietal Bowman capsule (29%, including using BK immunostains), crescents (12%) and glomerulonephritis (3%)
Microscopic (histologic) images

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Various images


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Figure 1: tubulointerstitial nephritis with lymphocytes and enlarged tubular epithelial cells
Figure 2: tubular cells have large smudged nuclei and basophilic chromatin
Figure 3: EM shows distinct intranuclear inclusion
Figure 4: inclusion consists of crystalline arrays of nonenveloped, round, electron dense particles, mean 45 nm in diameter, in loose crystalline lattices

Electron microscopy images

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Tubular cell with
numerous viral
particles (inset:
anti SV40 antibody)
Differential diagnosis
  • Other infection
  • Rejection