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Adverse Occurrence type:
To the author's knowledge, this is the first published case where the transmission of HHV8 from the donor has led to Kaposi's sarcoma (KS) in the recipient allograft (2008).
Time to detection:
Alerting signals, symptoms, evidence of occurrence:
Increasing creatinine level, rising to 157 mmol/L over the course of 1 month, edematous bulky transplant kidney (CT), dilated collecting system and mild obstruction (US, MAG3 renogram).
Demonstration of imputability or root cause:
Histological examination of the tumor showed a spindle cell mass adjacent to the ureteric lumen expressing CD34 and HHV8 antigen. Biopsy positive for HHV8 DNA using PCR. FISH evidence, demonstrating X and Y chromosomes in the majority of tumor cells strongly suggest that the tumor arose from HHV8 reactivation within the male donor tissue (the recipient was a 55-year-old female). Highly likely that the HHV8 was reactivated from within the donor tissue, permitted by the recipient’s immunosuppression, directly leading to KS formation. No pre-transplant serology done in donor and recipient to establish HHV8 serostatus. No epidemiological data described for donor and recipient. Discontinuation of mycophenolate mofetil and careful reduction of cyclosporin A led to tumor control and good graft function.
Suggest new keywords:
KS (Kaposi's sarcoma)
KSHV (Kaposi's sarcoma associated herpesvirus)
Dudderidge TJ, Khalifa M, Jeffery R, Amlot P, Al-Akraa M, Sweny P. Donor-derived human herpes virus 8-related Kaposi's sarcoma in renal allograft ureter. Transpl Infect Dis. 2008 Jun;10(3):221-6. Epub 2007 Dec 13.
Expert comments for publication:
Post transplant KS is more commonly due to reactivation in previously infected recipients but donor-derived infection is known to occur, leading to asymptomatic seroconversion, skin or multivisceral KS. Donor-derived KS of the allograft is less common. Stepwise and controlled alteration of immunosuppression has been succesfully used to control HHV8 and lead to tumor regression.