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• W2034761785 abstract "P817* Aims: We determined clinical and viral risk factors associated with the development of BK viruria, viremia, and sustained viremia in a prospective, randomized clinical trial of 200 consecutive de novo kidney transplant recipients. Methods: Clinical data was collected pre-transplant and during one year of follow-up. Urine and plasma were collected pre-transplant, weekly for 16 weeks, and at months 5, 6, 9, and 12. DNA extracted from plasma and urine was tested by real-time LightCycler PCR for the presence of BK DNA. Donor and recipient pre-transplant BK IgG antibody (Ab) titers were determined by enzyme immunoassay of plasma. A 577 bp region of the BK VP1 gene was sequenced from the first positive urine of recipients who received paired kidneys from the same donors. Results: Pre-transplant plasma samples were collected from 154 (77%) recipients and 72 (36%) donors including 66 donor-recipient pairs and 18 recipients of paired kidneys from 9 donors. In total, 7177 (85.4%) samples were collected. BK was detected in one or more urine specimens (viruria) in 70 (35.4%) of the 198 subjects who submitted samples. Twenty-three (11.6%) patients had BK detected in one or more plasma samples (viremia). Eleven patients (5.6%) had sustained viremia, defined as ≥2 consecutive BK positive samples spanning ≥3 weeks. Viremia never occurred without viruria. The onset of viruria was associated with a positive donor BK Ab status (p= 0.0002) and level of donor BK Ab titer (p<0.0001). The likelihood of developing viruria increased in a stepwise fashion from 0% with Ab titer <640 to 83% with Ab titer of 163,840. Neither recipient Ab status nor titer was associated with the onset of viruria or viremia (p>0.1). There was a trend toward an association between onset of viremia and donor Ab status (p=0.052). Viremia occurred in 20% of patients with HLA C7 in the donor or recipient and 7% without (p=0.005). Sustained viremia occurred in 14% of patients with HLA C7 in the donor or recipient and 1% without (p<0.0001). Twenty recipient pairs received kidneys from the same donors. BK infection in 16 pairs were concordant:10 pairs remained BK free, 5 pairs developed BK viruria, and 1 pair developed sustained viremia. Concordance among the pairs occurred more frequently than expected (p=0.022). Sequencing of the VP1 region of BK from the urine of the 6 concordant pairs who developed viruria revealed identical sequences within each pair. Conclusions: BK reactivation in the urine after kidney transplantation is more likely of donor origin and driven by donor antibody level, while progression to sustained viremia, a likely precursor to nephropathy, is dependant on the absence of HLA C7. The strong association of viruria with donor antibody titer, the concordant results of recipients of paired kidneys, and identical BK sequences in recipients of paired kidneys supports a donor origin for reactivated BK. Once BK has reactivated, recipient immunological susceptibility, perhaps indicated by the absence of HLA C7, allows for progression to sustained viremia." @default.
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• W2034761785 date "2004-07-01" @default.
• W2034761785 modified "2023-10-18" @default.
• W2034761785 title "HIGH DONOR ANTIBODY LEVEL AND HLA C7 PREDICT SUSTAINED BK-POLYOMA VIREMIA: RESULTS OF A RANDOMIZED PROSPECTIVE TRIAL" @default.
• W2034761785 doi "https://doi.org/10.1097/00007890-200407271-01313" @default.
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