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Updated: Aug 14, 2026

Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry
Published on: July 13, 2019
[BK virus infection in a pediatric renal transplant recipient]
R Bonaventura1, A Vázquez, A Exeni
1Servicio de Neurovirosis, Dpto Virología, INEI, ANLIS, Dr. C. Malbrin, Av. Velez Sarsfield 563 (1281) Capital Federal. rbonaventura@anlis.gov.ar
Insights
BK virus infection can cause kidney graft damage in pediatric transplant recipients. Differentiating BK virus infection from acute rejection is crucial for appropriate immunosuppressant management.
Area of Science:
- Nephrology
- Virology
- Immunology
Background:
- BK Human Polyomavirus establishes latency in the urinary tract after asymptomatic childhood infection.
- Reactivation of BK virus can cause renal pathology in immunocompromised individuals, especially pediatric transplant recipients.
Observation:
- A 5-year-old pediatric renal transplant recipient experienced graft dysfunction and renal failure episodes post-transplantation.
- Diagnostic investigations included analysis of blood, urine, renal biopsy, and lymphocele fluid.
- Differential diagnosis involved testing for BK virus, CMV, ADV, and cytological examination of renal tissue.
Findings:
- Clinical signs and laboratory results indicated BK virus infection as the cause of graft damage.
- The patient presented with recurrent renal function failure following kidney transplantation.
Implications:
- Accurate differentiation between BK virus infection and acute rejection is critical in pediatric transplant management.
- Treatment strategies, particularly immunosuppressant therapy, differ significantly based on the diagnosis.
- This case highlights the importance of vigilant monitoring for viral infections in immunosuppressed pediatric patients.
Abstract:
BK Human Polyomavirus causes an asymptomatic primary infection in children, then establishing latency mainly in the urinary tratt. Viral reactivation can lead to renal pathology in individuals with impaired cellular immune response. This is particularly important in pediatric transplant recipients, who can suffer a primary infection when immunosupressed. We followed up the case of a 5 years old patient who received a renal transplant in October 2003, and presented damaged graft 45 days after the intervention. The patient suffered 3 episodes of renal function failure between October 2003 and June 2004. Blood, urine, renal biopsy and lymphocele liquid samples were analyzed. A differential diagnosis between acute rejection and infectious causes was established by testing for BK, CMV and ADV viruses, and the cytological study of renal tissue. Laboratory findings together with clinical signs suggest the patient was infected by BK virus. As a final consideration, the great importance of differentiating between acute rejection and BK infection is emphasized, since immunosuppressant management is opposite in each case.
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