ESPN 51th Annual Meeting

ESPN 2018

Intrarenal viral infection and humoral rejection: a retrospective study in pediatric renal transplant recipients
Giulia Fregonese 1 Nicola Bertazza Partigiani 1 Andrea Carraro 1 Enrico Vidal 1 Susanna Negrisolo 1 Luisa Murer 1

1- University-Hospital of Padova, Pediatric Nephrology, Dialysis and Transplant Unit, Department of Women’s and Children’s Health, Padua, Italy

Humoral rejection represents one of the risk factors for reduced transplanted kidney survival. Different studies in literature have linked CMV and BK virus infections to humoral rejections.

Material and methods:

We led a retrospective study in pediatric recipients (m. age 11.1±6.9 y), transplanted at our Center from 2011 to 2016, to evaluate the possible correlation between acute/chronic humoral rejection and viral infections. Humoral rejection incidence has been calculated based on protocol biopsies performed at 6, 12 and 24 months after transplantation (Banff ’15) in association with anti-HLA antibodies (positive DSA: MFI>3000). Viral positivity (CMV, EBV, BKV, Parvovirus B19) was defined in two conditions: a) systemic with a persistent viremia for the 3 months preceding control biopsy; b) intrarenal with viral DNA isolation in bioptic tissue. The clinical samples considered were 175 protocol biopsies, 42 diagnosed as acute rejection and 6 as chronic rejection (75% cellular vs 25% humoral). 


The study has shown that there is no correlation between systemic viral infection and humoral or cellular rejection. Furthermore, our analysis emphasized that the localization of at least one graft-level virus is more correlated to humoral rejection than to cellular rejection (75%vs29%, p=0.04). In particular, the presence of Parvovirus B19 is highly associated with humoral rejection compared to the cellular one (50%vs13%, p=0.04). 


Our outcomes suggest a major risk of humoral rejection in patients with intrarenal infections. In particular, in transplanted patients Parvovirus B19 could increase the risk of humoral rejection, amplifying the exposition of MCH II antigens through INFy pathway.