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Effects of IVIG Therapy and FcγR Polymorphisms on BK Virus Nephropathy in Kidney Transplant Recipients

D. I. Min1, Y. Chang2, T. Shah3

1Western Univ of Health Sciences, Los Angeles, CA, 2Mendez National Institute of Transplantation Foundation, Los Angeles, CA, 3St. Vincent Medical Center, Los Angeles, CA

Meeting: 2019 American Transplant Congress

Abstract number: D402

Keywords: Gene polymorphism, IVIG, Polyma virus

Session Information

Session Name: Poster Session D: Late Breaking

Session Type: Poster Session

Date: Tuesday, June 4, 2019

Session Time: 6:00pm-7:00pm

 Presentation Time: 6:00pm-7:00pm

Location: Hall C & D

*Purpose: BK Virus Nephropathy (BKVN) is a major complication in kidney transplant patients. Although standard treatment for BKVN is immunosuppression reduction and/or using leflunomide, studies have shown benefit in using intravenous immunoglobulin (IVIG). Fcγ receptor (FcγR) genomic polymorphisms have also been associated with persistent BKVN. This study aims to investigate the efficacy of IVIG therapy on persistent BKVN with standard therapy and its association with FcγR genetic polymorphisms. It is hypothesized that IVIG therapy lowers BK DNA viral load, and FcγR polymorphisms are associated with persistent BKVN.

*Methods: A retrospective study was performed on 279 kidney transplant patients at St. Vincent Medical Center in Los Angeles, CA from January 2012 to December 2016. Among these, 193 patients were excluded for negative BKVN. The remaining 86 BKVN patients were separated into two groups: experimental group receiving IVIG and control group receiving standard therapy. Alleles of FcγR2A and FcγR3A were also included in the analyses. Chi-squared and student t-tests were used for comparison.

*Results: A total of 86 patients developed BK Viremia (30.8%). Among these, 52 patients received IVIG therapy and 34 patients received standard therapy. Overall, 90.4% of patients who received IVIG for BKVN responded to treatment (47/52). The BK DNA viral loads for IVIG responders were significantly lower than non-responders at time of diagnosis (29,816.3 vs. 219,271.8 copies/mL, p=0.013) and 6 months after IVIG use (1,369.5 vs 12,789.5 copies/mL, p=0.023). Analyses of FcγR2A (OR=0.807, CI[0.435-1.496], p=0.495) and FcγR3A alleles (OR=0.997, CI[0.505-1.970], p=0.993) showed no significant difference in all groups.

*Conclusions: IVIG appears to resolve BK viremia in the majority of severe BKVN patients. However, IVIG appears to be ineffective in patients with extremely high viral load at the diagnosis. Our study failed to show any associations between FcγR2A and FcγR3A with BKVN.

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To cite this abstract in AMA style:

Min DI, Chang Y, Shah T. Effects of IVIG Therapy and FcγR Polymorphisms on BK Virus Nephropathy in Kidney Transplant Recipients [abstract]. Am J Transplant. 2019; 19 (suppl 3). https://atcmeetingabstracts.com/abstract/effects-of-ivig-therapy-and-fc%ce%b3r-polymorphisms-on-bk-virus-nephropathy-in-kidney-transplant-recipients/. Accessed May 8, 2025.

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