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Blood, 15 September 2001, Vol. 98, No. 6, pp. 1971-1978
TRANSPLANTATION
Quantification of polyoma BK viruria in hemorrhagic cystitis
complicating bone marrow transplantation
Anskar Y. H. Leung,
Christine K. M. Suen,
Albert K. W. Lie,
Raymond H. S. Liang,
Kwok Y. Yuen, and
Yok L. Kwong
From the Department of Medicine, Queen Mary Hospital,
Hong Kong.
Polyoma BK virus (BKV) is frequently identified in the urine of
bone marrow transplantation (BMT) patients with hemorrhagic cystitis
(HC). However, viruria is common even in asymptomatic patients, making
a direct causative role of BKV difficult to establish. This study
prospectively quantified BK viruria and viremia in 50 BMT patients to
define the quantitative relationship of BKV reactivation with HC.
Adenovirus (ADV) was similarly quantified as a control. More than 800 patient samples were quantified for BKV VP1 gene with a
real-time quantitative polymerase chain reaction. Twenty patients
(40%) developed HC, 6 with gross hematuria (HC grade 2 or higher) and
14 with microscopic hematuria (HC grade 1). When compared with
asymptomatic patients, patients with HC had significantly higher peak
BK viruria (6 × 1012 versus 5.7 × 107
genome copies/d, P < .001) and larger total amounts of
BKV excreted during BMT (4.9 × 1013 versus
7.7 × 108 genome copies, P < .001). There
was no detectable increase in BK viremia. Binary logistic regression
analysis showed that BK viruria was the only risk factor, with HC not
related to age, conditioning regimen, type of BMT, and
graft-versus-host disease. Furthermore, the levels of ADV viruria in
patients with or without HC were similar and comparable with those of
BK viruria in patients without HC, suggesting that the significant
increase in BK viruria in HC patients was not due to background viral
reactivation or damage to the urothelium. BK viruria was quantitatively
related to the occurrence of HC after BMT.
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