Viral load and duration of BK polyomavirus viraemia determine renal graft fibrosis progression: histologic evaluation of late protocol biopsies
Abstrakt
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 viremia in the development and progression of interstitial fibrosis and tubular atrophy (IFTA).
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 viremia with 10 (5%) cases of polyomavirus-associated nephropathy.
Transient (=3 months) BKV viremia in 30%. A high viral load (>=10,000 copies/mL) was detected in 18%, 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, 12.1; 95% confidence interval, 1.62-90.0; P=0.015) or persistent BKV viremia (67%; odds ratio, 6.33; 95% confidence interval, 1.19-33.7; P=0.031) with corresponding rise in "interstitial fibrosis + tubular atrophy" scores. Only patients with transient low BKV viremia showed similar incidence and progression of IFTA as no-BKV group.
Persistent low BKV viremia was uncommon yet the progression of fibrosis was significant. Only recipients with polyomavirus-associated nephropathy experienced inferior graft survival at 5 years.
Conclusions. These data suggest only transient low BKV viremia does not negatively affect the progression of allograft fibrosis in contrast to excessive risk of severe fibrosis after high or persistent BKV viremia.