1. IL28B rs12979860 genotype as a predictor marker of progression to BKVirus Associated nephropathy, after kidney transplantation.
- Author
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Dvir R, Paloschi V, Canducci F, Dell'Antonio G, Racca S, Caldara R, Pantaleo G, Clementi M, and Secchi A
- Subjects
- Adult, Aged, Alleles, BK Virus growth & development, BK Virus pathogenicity, Biomarkers metabolism, Case-Control Studies, Disease Progression, Female, Gene Expression, Humans, Interferons, Interleukins immunology, Kidney Failure, Chronic genetics, Kidney Failure, Chronic immunology, Kidney Failure, Chronic pathology, Kidney Failure, Chronic surgery, Male, Middle Aged, Nephritis diagnosis, Nephritis immunology, Nephritis pathology, Polymorphism, Single Nucleotide, Polyomavirus Infections diagnosis, Polyomavirus Infections immunology, Polyomavirus Infections pathology, Prognosis, Transplantation, Homologous, Tumor Virus Infections diagnosis, Tumor Virus Infections immunology, Tumor Virus Infections pathology, Genetic Predisposition to Disease, Interleukins genetics, Kidney Transplantation adverse effects, Nephritis genetics, Polyomavirus Infections genetics, Tumor Virus Infections genetics
- Abstract
BK virus (BKV) associated nephropathy (BKVAN) is still an important cause of allograft dysfunction after kidney transplantation (KT). Recent data have shown that the new interferon (IFN)-λ family has been ascribed antiviral properties similar to IFNα, and that the response to IFNλ in kidney is restricted to epithelial cells, suggesting that the IFNλ system evolves as specific protection of the epithelia. We aimed to test the hypothesis of correlation between a single nucleotide polymorphism (C/T dimorphism rs12979860) in the genomic region of IL28B and BKVAN, in patients after KT. Fifty kidney-transplanted patients were included as follow: Group 1 (BKV+/BKVAN+): 11 patients with active BKV- replication and biopsy-proven BKVAN; Group 2 (BKV+/BKVAN-): 22 patients with active BKV- replication but without evidence of BKVAN; Group 3 (BKV-/BKVAN-): 17 patients without evidence of BKV- replication (control group). Here we show that the C/C genotype was statistically higher in group 2 than in group 1 and BKVAN was detected significantly more frequently in patients with C/T and T/T genotypes than in patients with C/C genotype. We therefore propose IL28B polymorphism (rs12979860), as a predictor-marker to differentiate between patients with self-limited, even if persistent, BKV- reactivation and patients with a high risk of progression towards BKVAN, and to modulate the clinical management of these patients accordingly.
- Published
- 2017
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