RESEARCH ARTICLE
Significance of Asymptomatic Persistent Epstein-Barr Viral Load in Pediatric Renal Transplant Recipients: North American Pediatric Renal Trials and Collaborative Studies Report
Asha Moudgil1, Karen Martz2, Therese Moore3, William E. Harmon4, Vikas R. Dharnidharka5, *
Article Information
Identifiers and Pagination:
Year: 2014Volume: 7
First Page: 123
Last Page: 128
Publisher ID: TOUNJ-7-123
DOI: 10.2174/1874303X014070100123
Article History:
Received Date: 25/9/2014Revision Received Date: 1/10/2014
Acceptance Date: 2/10/2014
Electronic publication date: 31 /12/2014
Collection year: 2014
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/) which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background:
Many pediatric transplant (TX) centers routinely monitor Epstein-Barr (EB) viral load (VL) by real time quantitative PCR and intervene to prevent post-transplant lymphoproliferative disorder (PTLD). Some children develop asymptomatic persistent VL (PVL). Outcome of different interventions in preventing PTLD and other undesired effects on acute rejection (AR), graft failure (GF) and function amongst children with asymptomatic PVL is not known.
Methods:
NAPRTCS centers invited to enter data on children with asymptomatic PVL (≥ 6 months) into the EB VL registry. Comparison group included children into the NAPRTCS TX arm during the same period without PVL or VL monitoring. EB VL were arbitrarily divided into low (1-10), medium (>10-100) and high (>100times detection limit for the center) ratio.
Results:
Of 645 children (18 centers), 85 (13.2%) developed onset of PVL at a mean of 6.4 ± 6.3 months post-TX. PVL children were more likely to be younger (< 5 years) at TX and less likely to be African-American and majority (75.3%) was mismatched for EBV (donor EBV IgG positive and recipient negative). Thymoglobulin induction was used in 29.4% children with PVL versus 37% in controls (p=ns). PTLD developed in 7/85 (8.2%) children with PVL versus 5/560 (0.9%) controls (p < 0.0001). EB VL ratios were not different in those with and without PTLD. EB PVL as time varying covariate did not affect patient survival, GF and AR (HR, 0.85, 0.53 and 0.99). The change in GFR overtime in children with PVL was comparable to controls.
Conclusion:
Children with PVL (actual load not predictive) are at increased risk for PTLD, but not for AR, death, GF or loss of graft function.
