RESUMO
Hemorrhagic cystitis [HC] in allogeneic bone marrow transplanted [BMT] patients is associated with BK virus [BKV] reactivation manifested as BK viruria. However, since 77-90% of all adult BMT patients excrete BKV, viral reactivation alone cannot be responsible for HC. Recently, a significant overrepresentation of C[right arrow]G mutations in the Sp1 binding site in the non-coding control region [NCCR] of BKV was shown to be present in HC patients and absent in non-HC patients. We aimed to investigate if this mutation resulted in excessive BKV excretion in HC patients. Study design: A Real-Time PCR was developed and used to quantify BKV in urine samples from 21 patients with HC, with and without the mutations, as well as from patients without HC. A Real-Time PCR was developed and used to quantify BKV in urine samples from 21 patients with HC, with and without the mutations, as well as from patients without HC. Quantification of BKV was successful in 18 of 21 urine patients [six with and six without C[right arrow]G mutations] and six patients without HC. A mean of 3.0x10[6] BKV copies/micro was detected in urine samples of HC patients with C[right arrow]G mutations, compared to a mean of 1.5*10[6] BKV copies/micro L in HC patients without C[right arrow]G mutations and a mean of 10x10[6] BKV copies/ micro L in patients without HC. The obtained differences were however not statistically significant, due to one individual non-HC patient with an extremely high BKV copy number. Nevertheless, while 50% of the samples in the HC groups expressed 1*10[6] copies/micro L or more, only one of the samples in the non-HC group contained a virus quantity higher than 5* 10[5] copies. Although we could not confirm that the C[right arrow]G mutations in the Sp1 site of BKV were responsible for an increased viral load in patients with HC, our data suggest that levels of BKV above 10[4] copies/ micro L may indicate a risk for HC