Abstract

The BK virus (BKV) produces a subclinical kidney infection in immunocompetent individuals. However, viremia may occur in kidney transplant patients with ongoing immunosuppression. BKV-associated nephropathy (BKVN) has no specific treatment and is a leading cause of organ transplant loss. In this study, we evaluated the predisposition and the clinical impact of BKV replication in kidney transplant patients during post-transplant monitoring in a reference institution in Brazil. Demographic, clinical and laboratory data generated during routine outpatient follow-up were retrospectively collected. BK viremia was investigated using real-time polymerase chain reaction. Of the 553 participants, 7.4% (n = 41) presented BKV replication. Of these, 16 (39%) lost their kidney graft and interstitial nephritis was identified on kidney biopsy in 50% of the cases. Among the evaluated variables, only the use of the immunosuppressant mycophenolate sodium was identified as a risk factor for viremia (OR 7.96; 95% CI 2.35 to 26.98). The graft survival estimate in BKV-positive patients was significantly reduced (24.8% vs. 85.6%) after 10 years of transplantation. We concluded that defining predisposing factors remains an important challenge for the prevention and control of BKV activity following kidney transplantation, especially considering the development of BKVN and its strong effect on graft maintenance.

Highlights

  • Kidney transplantation is considered to be the best method of treatment for patients with chronic kidney failure

  • Reactivation of the polyomavirus only occurs in cases of autoimmune disease and in immunocompromised individuals, such as those infected with the human immunodeficiency virus (HIV) and solid organ transplant patients because these conditions involve altered immune systems (Manitpisitkul et al 2009)

  • Post-transplant BKV-associated nephropathy (BKVN) is a major cause of graft dysfunction and loss (Siguier et al 2012, Mbianda et al 2015)

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Summary

Introduction

Kidney transplantation is considered to be the best method of treatment for patients with chronic kidney failure. The recurrence of chronic nephropathy and both long and short term graft loss have been attributed to the development of opportunistic infections, especially BK virus (BKV) infection (Egli et al 2007). Reactivation of the polyomavirus only occurs in cases of autoimmune disease and in immunocompromised individuals, such as those infected with the human immunodeficiency virus (HIV) and solid organ transplant patients because these conditions involve altered immune systems (Manitpisitkul et al 2009). BKVN may cause graft dysfunction, premature failure and loss (Hirsch et al 2013). All kidney transplant recipients with BKV replication have variable deteriorating graft function, which is manifested as an increase in serum creatinine (Ramos et al 2002). The immunosuppression load administered after transplantation has been reported to be the primary risk factor for BKVN development (Boothpur and Brennan 2010)

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