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Kidney Week

Abstract: PO0219

BK Polyomavirus Nephritis in a Low-Risk Native Kidney: A Case Report

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention


  • Saleem, Maryam, Washington University in St Louis, St Louis, Missouri, United States
  • Khoury, Charbel C., Washington University in St Louis, St Louis, Missouri, United States

BK viremia has increased prevalence in solid organ transplant, particularly renal transplant recipients. BK nephropathy in native kidney is rare, but has been reported after hematopoietic stem cell transplant (HSCT).

Case Description

74-year-old male with Grade 2 Follicular lymphoma (in complete remission for 2 years after obinutuzumab, bendamustine, & venetoclax), complicated by hypogammaglobinemia receiving IVIG (IgG 751mg/dL) & chronic lymphopenia(absolute lymphocyte 152 cells/uL) who was evaluated for acute kidney disease. Patient’s baseline creatinine was around 0.8 mg/dL & progressively rose to 4mg/dL over a period of 6 months despite IV hydration for intermittent mild diarrhea. Urinalysis had no proteinuria or hematuria. Serologic workup for systemic lupus erythematosus and other autoimmune disease, monoclonal gammopathy, sarcoid was unrevealing. Kidney biopsy revealed polyomavirus nephritis with acute tubular injury & severe interstitial fibrosis with tubular atrophy. Serum BK PCR showed 1.3 million copies. The patient continued on IVIG increasing the frequency to every 3 weeks and started on a course of fluoroquinolones but with ultimate progression to chronic kidney disease.


BK virus infections in immunocompetent individuals typically occur early in childhood (asymptomatic or mild respiratory illness). Following primary infection, BK virus remains in a latent state in the urothelium & renal tubular epithelial cells. Most cases of BK Polyomavirus nephritis occur in renal transplant recipients. Risk factors for BK Polyomavirus nephritis in native kidneys include non-renal solid organ transplant as well as HSCT, chronic lymphocytic leukemia, AIDS, and congenital dysgammaglobulinemia. Clinical presentation is nonspecific and includes varying degrees of renal failure without fever, leukocytosis, hematuria or proteinuria. Incidence of renal failure is dependent on the degree of glomerular inflammation caused by proinflammatory cytokines, influx of immune effector cells, BK virus lytic replication, and lysis of renal tubular epithelial cells that can lead to renal fibrosis. Treatment agents include leflunomide, cidofovir, fluoroquinoles and IVIG but the success has been limited. This case highlights that BK nephropathy may develop in the native kidney other than HSCT. Chronic lymphopenia & hypogammaglobinemia likely predisposed our patient despite his ongoing infusion of IVIG.