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BK Virus Nephropathy: Histological Evolution by Sequential Pathology
Author(s) -
Nankivell B. J.,
Renthawa J.,
Sharma R. N.,
Kable K.,
O'Connell P. J.,
Chapman J. R.
Publication year - 2017
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.14292
Subject(s) - medicine , histopathology , bk virus , viremia , pathology , nephropathy , fibrosis , inflammation , kidney , virus , gastroenterology , kidney transplantation , immunology , diabetes mellitus , endocrinology
Reactivation of BK virus in renal allografts causes a destructive chronic infection. This single‐center retrospective cohort study describes the evolution of BK virus allograft nephropathy ( BKVAN ) from 63 kidneys (from 61 patients) using sequential histopathology (454 biopsies, averaging 7.8 ± 2.6 per kidney) followed for 60.1 mo. Uninfected protocol biopsies formulated time‐matched control Banff scores (n = 975). Interstitial inflammation occurred in 73% at diagnosis, correlating with viral histopathology (r = 0.413, p = 0.008) and amplifying early injury with accelerated interstitial fibrosis and tubular atrophy ( IF / TA , p = 0.017) by 3 mo. Prodromal simian virus 40 large T antigen ( SV 40T)–negative inflammation with viremia preceded the histological diagnosis in 23.8%. Persistent subacute injury from viral cytopathic effect was associated with acute tubular necrosis and ongoing interstitial inflammation, culminating in IF / TA in 86.9%. Overall, cellular interstitial infiltration mitigated the intensity of subsequent tubular injury, SV 40T, and tissue viral load, assessed by sequential paired histology (p < 0.001). Graft loss was predicted by high‐level viremia (hazard ratio [ HR] 4.996, 95% CI 2.19–11.396, p < 0.001), deceased donor ( HR 3.201, 95% CI 1.149–8.915, p = 0.026), and late acute rejection ( HR 3.124, 95% CI 1.037–9.413, p = 0.043). Transplant failure occurred in 38.1%, with uncontrolled infection (58.3%) and SV 40T‐negative chronic rejection (41.7%) causing losses. BKVAN is characterized by subacute virus‐induced tubular injury, inflammation, and progressive nephron destruction. Effective antiviral therapy remains an unmet clinical need.

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