Adenovirus infection is associated with graft dysfunction and graft loss in pediatric cardiac, lung, and liver transplants in prior retrospective studies, but data in pediatric kidney transplant recipients is limited.
We conducted a prospective single-center cohort study of 75 consecutive pediatric kidney transplant recipients who underwent monthly screening for adenovirus viremia and symptom assessment for 2 years posttransplant.
Adenovirus viremia was detected in 11 (14.7%) patients at a median onset of 173 days (interquartile range, 109-310 days) posttransplant, 6 (8%) had asymptomatic viremia, and 5 (6.7%) had symptomatic disease (2 with hematuria and 3 with an acute febrile respiratory illness). Viremic patients did not differ from nonviremic patients in age, immunosuppression management, or cytomegalovirus or Epstein-Barr virus serostatus, but were more likely to develop cytomegalovirus viremia during the first 2 years posttransplant. No patient had an increase in creatinine from baseline during the time of adenovirus viremia. In a Cox proportional hazards regression, subclinical adenovirus viremia was not associated with a faster time to a 30% decline in estimated glomerular filtration rate.
Adenovirus infection is common among pediatric kidney transplant recipients and frequently causes symptomatic disease; however, symptoms are often mild and are not associated with a decline in graft function. Routine monitoring for adenovirus viremia in pediatric kidney transplant recipients may not be warranted.
This prospective study shows that adenovirus viremia occurs in 15% of pediatric kidney transplant recipients. It is symptomatic in half of those who are viremic and mildly symptomatic in the other half. The authors conclude that routine monitoring for adenovirus viremia in pediatric kidney transplant recipients may not be warranted.
1 Department of Pediatrics, University of Washington, Seattle, WA.
2 Fred Hutchinson Cancer Research Center, Seattle, WA.
3 Department of Laboratory Medicine, University of Washington, Seattle, WA.
4 Division of Nephrology, Seattle Children’s Hospital Seattle, WA.
Received 16 August 2017. Revision received 16 November 2017.
Accepted 9 December 2017.
This research was supported by NIH grant 5 T32 DK007662.
The authors declare no conflicts of interest.
R.M.E. participated in the research design, performance of the research, writing of the article, and data analysis. M.-L.H. participated in the performance of the research and writing of the article. G.P. participated in the performance of the research. J.M.S. participated in the research design, writing of the article, performance of the research, and data analysis. A.P.L. participated in the research design, performance of the research, and writing of the article.
Correspondence: Rachel M. Engen, MD, MS, Children's Hospital of Chicago, 225 E Chicago Ave, Box 37, Chicago, IL 60611. (firstname.lastname@example.org).