Abstract
Acute renal dysfunction (ARD) is a common complication in renal transplant recipients. Multiple factors contribute to ARD development, including acute rejection and microbial infections. Many viral infections after kidney transplantation result from reactivation of “latent” viruses in the host or from the graft, such as the human Polyomavirus BK (BKV). We report the case of a 39 year-old recipient of a 2nd kidney graft who experienced BKV reactivation after a second episode of acute humoral rejection. A 10-day treatment with the quinolone antibiotic ciprofloxacin was administered with an increase of immunosuppressive therapy despite the active BKV replication. Real Time PCR analysis performed after treatment with ciprofloxacin, unexpectedly showed clearance of BK viremia and regression of BK viruria. During the follow-up, BK viremia persisted undetectable while viruria decreased further and disappeared after 3 months.BKV non-coding control region sequence analysis from all positive samples always showed the presence of archetypal sequences, with two single-nucleotide substitutions and one nucleotide deletion that, interestingly, were all representative of the subtype/subgroup I/b-1 we identified by the viral protein 1 sequencing analysis.We report the potential effect of the quinolone antibiotic ciprofloxacin in the decrease of the BKV load in both blood and urine.
Highlights
Acute renal dysfunction (ARD) is a common complication in renal transplant recipients
Most viral infections after renal transplantation result from reactivation of “latent” viruses in the host or from the graft, such as the human Polyomavirus BK (BKV) [2]
In this report we describe the case of a highly sensitized kidney re-transplant patient who needed an overall increase of immunosuppression, due to acute rejection, in course of ARD associated to BKV reactivation
Summary
Acute renal dysfunction (ARD) is a common complication in renal transplant recipients. In this report we describe the case of a highly sensitized kidney re-transplant patient who needed an overall increase of immunosuppression, due to acute rejection, in course of ARD associated to BKV reactivation. Donor Specific Antibodies (DSA) before his second transplant were not detectable and the cross-match was negative as well He received induction therapy with basiliximab at standard dosage and maintenance triple therapy with Tac (trough levels: 4–8 ng/mL), MMF and steroids. We performed the molecular characterization of the BKV viral protein 1 (VP1) and noncoding control region (NCCR) on the urine and blood samples which were positive for viral DNA during the follow-up Both regions, amplified by specific nested PCR and sequenced using a dedicated facility, were analysed to classify the BKV strains obtained into the corresponding subtype/subgroup, examining the single nucleotide polymorphisms within the VP1 region, and to investigate the presence of possible rearrangements within the NCCR. All BKV strains isolated in both urine and blood belonged to the archetype strains (WW), with VP1 genotype defined as subtype I/subgroup b-1
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