Viral load and duration of BK polyomavirus viremia determine renal graft fibrosis progression: histologic evaluation of late protocol biopsies

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00669806%3A_____%2F19%3A10400750" target="_blank" >RIV/00669806:_____/19:10400750 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11140/19:10400750

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=G3nO-xq_LN" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=G3nO-xq_LN</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1093/ndt/gfz061" target="_blank" >10.1093/ndt/gfz061</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Viral load and duration of BK polyomavirus viremia determine renal graft fibrosis progression: histologic evaluation of late protocol biopsies

Popis výsledku v původním jazyce

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 (&lt;3 months) BKV viremia occurred in 70% patients while persistent (&gt;=3 months) BKV viremia in 30%. A high viral load (&gt;=10,000 copies/mL) was detected in 18%, a low viral load (&lt;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 &quot;interstitial fibrosis + tubular atrophy&quot; 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.

Název v anglickém jazyce

Viral load and duration of BK polyomavirus viremia determine renal graft fibrosis progression: histologic evaluation of late protocol biopsies

Popis výsledku anglicky

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 (&lt;3 months) BKV viremia occurred in 70% patients while persistent (&gt;=3 months) BKV viremia in 30%. A high viral load (&gt;=10,000 copies/mL) was detected in 18%, a low viral load (&lt;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 &quot;interstitial fibrosis + tubular atrophy&quot; 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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30217 - Urology and nephrology

Projekt

<a href="/cs/project/LO1503" target="_blank" >LO1503: BIOMEDIC</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Nephrology, Dialysis, Transplantation

ISSN

0931-0509

e-ISSN

—

Svazek periodika

34

Číslo periodika v rámci svazku

11

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

1970-1978

Kód UT WoS článku

000498168100023

EID výsledku v databázi Scopus

2-s2.0-85073979583