Abstract
SummaryIn kidney transplant recipients (KTRs), BK polyomavirus (BKPyV) replication may progress to polyomavirus‐associated nephropathy (PVAN). In this retrospective study, we assessed the chemokine CXCL10 in urine and blood samples consecutively acquired from 85 KTRs who displayed different stages of BKPyV replication and eventually developed PVAN. In parallel to progression toward PVAN, CXCL10 gradually increased in blood and urine, from baseline (prior to virus replication) to BKPyV DNAuria (median increase in blood: 42.15 pg/ml, P = 0.0156), from mere DNAuria to low‐ and high‐level BKPyV DNAemia (median increase: 52.60 and 87.26 pg/ml, P = 0.0010 and P = 0.0002, respectively) and peaked with histologically confirmed PVAN (median increase: 145.00 pg/ml, P < 0.0001). CXCL10 blood and urine levels significantly differed among KTRs with respect to simultaneous presence of human cytomegalovirus (P < 0.001) as well as in relation to the clinical severity of respective BKPyV DNAemia episodes (P = 0.0195). CXCL‐10 concentrations were particularly lower in KTRs in whom BKPyV DNAemia remained without clinical evidence for PVAN, as compared to individuals who displayed high decoy cell levels, decreased renal function and/or biopsy‐proven PVAN (median blood concentration: 266.97 vs. 426.42 pg/ml, P = 0.0282). In conclusion, in KTRs CXCL10 rises in parallel to BKPyV replication and correlates with the gradual development of PVAN.
Highlights
BK virus (BKPyV) and JC virus (JCPyV), two human polyomaviruses, cause persistent infection, with the urinary tract as most relevant latency site [1]
We analyzed whether progression of BK polyomavirus (BKPyV) replication toward DNAemia and polyomavirus-associated nephropathy (PVAN) was associated with a response of the inflammatory chemokine CXCL10
We analyzed whether progression of BKPyV replication toward DNAemia and PVAN was associated with an inflammatory CXCL10 response in urine analogously to blood concentrations
Summary
BK virus (BKPyV) and JC virus (JCPyV), two human polyomaviruses, cause persistent infection, with the urinary tract as most relevant latency site [1]. Transplant International published by John Wiley & Sons Ltd on behalf of Steunstichting ESOT. Additional correlates of clinical progression are emergence of decoy cells in the urinary sediment, an indicator for cytopathic effects due to urothelial cell infection, the detection of viral aggregates by the Haufen test, BKPyV VP1 mRNA as well as histological evidence of viral inclusions, tubular injury, and inflammatory infiltrates [2,3,4,16,17,18]
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