BK Polyoma Virus Nephropathy in Hematopoietic Cell Transplant Recipients with Renal Dysfunction

BACKGROUND: BK polyoma virus (BKV) nephropathy (BKVN) is a well-established cause of allograft loss after kidney transplantation. In contrast BKVN is rarely been reported in hematopoietic cell transplant (HCT) recipients. Renal dysfunction after HCT is common and often attributed to total body irradiation, drug toxicity, hypertension or microangiopathy. As kidney biopsies are rarely performed after HCT, BKVN may be underdiagnosed. We report a Single-center experience of BKVN in HCT recipients. METHODS: Retrospective chart review of HCT recipients from January 1, 2016 through March 31, 2017. Only cases of BKVN confirmed by immunohistochemical stain on renal biopsy are included. Urine and blood BKV PCR was performed at Viracor Eurofins (Lee’s Summit, MO). Glomerular filtration rate (GFR) was estimated by Chronic Kidney Disease Epidemiology Collaboration equation. RESULTS: From 2016 to 2017, 320 patients received HCT and 6 patients underwent kidney biopsy and 4 had BKVN. Patient characteristics are shown in Table 1. Three patients (75%) received ex vivo T-cell depleted (CD34+ selected) peripheral blood (PB) HCT and did not receive pharmacologic GVHD prophylaxis; one patient received cord blood allograft. All patients had BKV viruria with a median BKV viral load of 9.3 log(10) copies/mL (range, 8.6–10.0) and median onset 18 days (range 6–41) post HCT. BKVN was diagnosed at a median of 275.5 days post-HCT (range, 141–637). All patients presented with decreased GFR (median 47.5% reduction, range 16–75%) from GFR at transplant. One patient had proteinuria (3 g over 24 hours); one patient had hydronephrosis. At BKVN diagnosis plasma BKV viral load was a median of 6.2 log(10) copies/mL; range, 6.0–6.3), absolute lymphocyte count median 1027 (range 335–2,536) and CD4+ lymphocyte count median 145 (range 64–172). CONCLUSION: (1) BKVN should be considered in HCT recipients with worsening renal function and high BKV viremia. (2) Early, noninvasive predictors of BKVN could aid in identifying high-risk patients for early intervention prior to irreversible loss of kidney function. (3) Reduction of immunosuppression is often not feasible in HCT. The role of preemptive antiviral therapy and/or adoptive cell therapy for BKV viremia in HCT should be evaluated in clinical trials. DISCLOSURES: G. Papanicolaou, Chimerix: Consultant, Grant Investigator and Investigator, Consulting fee, Grant recipient and Research grant