Viral load and duration of BK polyomavirus viraemia determine renal graft fibrosis progression: histologic evaluation of late protocol biopsies
Language English Country Great Britain, England Media print
Document type Clinical Trial, Journal Article, Research Support, Non-U.S. Gov't
PubMed
31071208
DOI
10.1093/ndt/gfz061
PII: 5435705
Knihovny.cz E-resources
- Keywords
- BK polyomavirus, BKV viraemia, fibrosis, renal transplantation, viral load,
- MeSH
- Fibrosis etiology pathology MeSH
- Transplantation, Homologous MeSH
- Tumor Virus Infections complications virology MeSH
- Middle Aged MeSH
- Humans MeSH
- Kidney Diseases etiology pathology MeSH
- Polyomavirus Infections complications virology MeSH
- Graft Survival MeSH
- Disease Progression MeSH
- Prospective Studies MeSH
- Virus Replication MeSH
- Kidney Transplantation adverse effects MeSH
- Viremia complications virology MeSH
- Viral Load * MeSH
- BK Virus isolation & purification pathogenicity MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Clinical Trial MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: Polyomavirus BK (BKV) infection of the renal allograft causes destructive tissue injury with inflammation and subsequent fibrosis. METHODS: Using a prospective cohort of patients after kidney transplantation performed between 2003 and 2012, we investigated the role of BKV viraemia in the development and progression of interstitial fibrosis and tubular atrophy (IFTA). The primary outcome was moderate-to-severe IFTA assessed by protocol biopsy at 36 months. RESULTS: A total of 207 consecutive recipients were enrolled. Of these, 57 (28%) developed BKV viraemia with 10 (5%) cases of polyomavirus-associated nephropathy (PVAN). Transient (<3 months) BKV viraemia occurred in 70% of patients, and persistent (≥3 months) BKV viraemia in 30%. A high viral load (≥10 000 copies/mL) was detected in 18% and a low viral load (<10 000 copies/mL) in 61%, while the viral load could not be determined in 21%. Moderate-to-severe IFTA was significantly increased in high [71%; odds ratio (OR) = 12.1; 95% confidence interval (CI) 1.62-90.0; P = 0.015] or persistent BKV viraemia (67%; OR = 6.33; 95% CI 1.19-33.7; P = 0.031) with corresponding rise in 'interstitial fibrosis + tubular atrophy' scores. Only patients with transient low BKV viraemia showed similar incidence and progression of IFTA to the no-BKV group. Persistent low BKV viraemia was uncommon yet the progression of fibrosis was significant. Only recipients with PVAN experienced inferior graft survival at 5 years. CONCLUSIONS: These data suggest that only transient low BKV viraemia does not negatively affect the progression of allograft fibrosis in contrast to excessive risk of severe fibrosis after high or persistent BKV viraemia.
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