Nephrotoxicity of calcineurin inhibitors as a risk factor for BK polyomavirus replication after kidney transplantation
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
32940913
DOI
10.1002/jmv.26520
Knihovny.cz E-resources
- Keywords
- BK polyomavirus-associated nephropathy, calcineurin inhibitors, kidney transplantation, nephrotoxicity, protocol biopsy,
- MeSH
- Biopsy MeSH
- Adult MeSH
- Immunosuppression Therapy MeSH
- Incidence MeSH
- Tumor Virus Infections virology MeSH
- Calcineurin Inhibitors adverse effects MeSH
- Kidney drug effects pathology virology MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Kidney Diseases chemically induced MeSH
- Polyomavirus Infections blood urine virology MeSH
- Transplant Recipients MeSH
- Prospective Studies MeSH
- Virus Replication drug effects MeSH
- Risk Factors MeSH
- Aged MeSH
- Kidney Transplantation adverse effects MeSH
- Viremia MeSH
- BK Virus drug effects physiology MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Calcineurin Inhibitors MeSH
BK polyomavirus-associated nephropathy (PyVAN) is responsible for a significant percentage of transplanted kidneys prematurely terminating their function. Its occurrence is closely related to the intensity of immunosuppressive therapy. In a group of 161 newly transplanted patients, we prospectively evaluated 457 protocol renal biopsies performed within the first year after transplantation. Using the calcineurin inhibitors (CI) nephrotoxicity score, the incidence of nephrotoxicity was monitored as a manifestation of excessive immunosuppression. Findings were correlated with clinical evidence of active BK polyomavirus (BKPyV) replication and PyVAN. Compared to the normal histology, nephrotoxicity was associated with more frequent BKPyV viremia and viruria (p = .01 and p < .01, respectively) and more common occurrence of PyVAN. The persistence of toxicity in the subsequent biopsy proved to be a negative risk factor of viremia and viruria (p = .03 and p < .01, respectively), independently of the initial BKPyV status. Toxicity could also be used as a predictor of viremia and viruria (p = .04 and p < .01, respectively) even in the absence of viral replication at the time of initial biopsy. The early histological manifestation of CI nephrotoxicity was associated with significant BKPyV reactivation in the risky first posttransplant year.
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