Kidney Week

Abstract: SA-PO1001

An Unusual Suspect: A Case of BK Nephropathy (BKVN)

Session Information

• Transplantation: Clinical - 4
  October 26, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Transplantation

• 2102 Transplantation: Clinical

Authors

• Huang, Gaoyuan, University of Washington School of Medicine, Seattle, Washington, United States

Gaoyuan Huang, MD, MS

• Bodell, Mabel Amelia, Confluence Health, Wenatchee, Washington, United States

Mabel Amelia Bodell, MD

• Patel, Aanand A., University of Washington School of Medicine, Seattle, Washington, United States

Aanand A. Patel, MD, PhD

• Akilesh, Shreeram, University of Washington School of Medicine, Seattle, Washington, United States

Shreeram Akilesh, MD, PhD

• Ng, Yue-Harn, University of Washington School of Medicine, Seattle, Washington, United States

Yue-Harn Ng, MD, MPH

• de Wolski, Karen S., University of Washington School of Medicine, Seattle, Washington, United States

Karen S. de Wolski, MD

Introduction

BK viral reactivation is known to occur in non-kidney solid organ transplant (NKSOT) recipients, but patients are not routinely screened for BK viremia/viruria, nor are there studies of the associated long-term kidney prognosis. Importantly, chronic kidney disease (CKD) in Orthotopic Heart-transplant (OHT) patients is often attributed to other causes, such as calcineurin-inhibitor (CNI) toxicity, leading to late or missed diagnosis of BKVN. Here, we report a case of BKVN of native kidneys causing advanced CKD in an OHT recipient.

Case Description

A young male with a history of OHT for viral cardiomyopathy 7 years prior and CKD initially attributed to CNI use (serum creatinine [SCr] 1.3-1.5mg/dl) was referred to nephrology for an increase in SCr to 3.8 over the last year. He had been on immunosuppression (IS) with tacrolimus (goal 8-10ng/ml) and mycophenolate (MMF). Due to concern for CNI toxicity, IS was switched to a CNI minimization regimen with reduction in tacrolimus, continuation of MMF, and addition of sirolimus one year before. However, Scr continued trending up and proteinuria increased to 3g/d, with otherwise bland urine and negative serologic workup, so sirolimus was discontinued. Unfortunately, kidney function continued to decline rapidly, prompting renal biopsy, which showed BKVN (Figure 1) with both chronic and active tubulointerstitial nephritis, 90% globally sclerosed glomeruli, and evidence of mild CNI toxicity. He was concurrently found to have high-titer BK viremia and viruria. MMF was reduced by 50%. He is starting dialysis.
OHT has been functioning well without rejection based on routine TTE and endomyocardial biopsies. He will not be a candidate for kidney transplant until resolution of BK viremia.

Discussion

Due to a lack of routine screening, BKVN of native kidneys may be an underreported etiology of CKD in NKSOT patients. Delayed diagnosis of BKVN can result in ESKD and be a barrier for kidney transplant, as is seen here. There may be a role for BK screening in NKSOT patients with kidney dysfunction as a means of early diagnosis of BKVN.