BK Virus and Cytomegalovirus Coinfections in Kidney Transplantation and Their Impact on Allograft Loss.

Sabina Herrera,Asunción Moreno,Frederic Cofan,Maria Angeles Marcos,Fritz Diekmann,Marta Bodro,Javier Bernal-Maurandi,Pedro Ventura,Laura Linares,Genoveva Cuesta

doi:10.3390/jcm10173779

Abstract

We aimed to ascertain the interaction and effects of combined reactivations of BK virus and cytomegalovirus on kidney graft function. All consecutive kidney transplant recipients (KTR) between 2003 and 2016 were included. Of 1976 patients who received a kidney transplant, 23 (1.2%) presented BKV-associated nephropathy (BKVAN). Factors independently associated with BKVAN were diabetes mellitus (odds ratios (OR) 3.895%, confidence intervals (CI) (1.4–10.5)), acute allograft rejection (OR 2.8 95%, CI (1.1–7.6)) and nephrostomy requirement (OR 4.195%, CI (1.3–13)). Cytomegalovirus infection was diagnosed in 19% of KTR patients. Recipients with BKVAN presented more frequently with cytomegalovirus (CMV) infection compared to patients without BKVAN (39% vs. 19%, p = 0.02). Acute allograft rejection (OR 2.95%, CI (1.4–2.4)) and nephrostomy requirement (OR 2.95%, CI (1.2–3)) were independently associated with CMV infection. Sixteen patients (69%) with BKVAN had graft dysfunction at one-year post-transplant and eight of them (35%) lost their graft. Patients presenting with BKVAN and graft loss presented more frequently a cytomegalovirus infection (OR 2.295%, CI (1.3–4.3)). In conclusion, we found a relation between CMV infection and graft loss in patients presenting BKVAN, suggesting that patients with CMV reactivation should be actively screened for BKV.

Highlights

Infection caused by BK polyomavirus (BKV) is acquired in childhood
BKV reactivation can manifest as viruria in 30% to 40% of kidney transplant recipients (KTR), viremia in 10% to 20% or BKV-associated nephropathy in 1% to 10% of patients according to published series [3,4]
In our study of a large cohort of KTR patients, we found that diabetes mellitus, acute allograft rejection and nephrostomy requirement were associated with BKV-associated nephropathy (BKVAN)

Summary

Introduction

Infection caused by BK polyomavirus (BKV) is acquired in childhood. The virus infects target tissues and remains latent in the kidneys in immunocompetent hosts. Reactivation occurs in the setting of immunosuppression, in cases where cellular immune responses are weakened [1]. In this scenario, replication in the graft begins, followed by expansion in the urine and eventually viremia. The interstitial tubules are the most frequent target of BKV, resulting in tubulointerstitial nephritis [2]. BKV reactivation can manifest as viruria in 30% to 40% of kidney transplant recipients (KTR), viremia in 10% to 20% or BKV-associated nephropathy in 1% to 10% of patients according to published series [3,4]

Objectives

Methods

Findings

Conclusion