BK Viremia Was Not Associated with Acute Kidney Injury in Hematopoietic Cell Transplant Recipients

Abstract

Introduction Acute kidney injury (AKI) is common in hematopoietic cell transplant (HCT) recipients. Few studies have evaluated whether BK polyomavirus (BKV) infections are associated with kidney disease in the HCT population, and results have not been conclusive. Objectives Using retrospectively collected BK plasma viral loads from a large cohort of HCT recipients, we assessed the relationship between plasma BKV replication and AKI through an analysis of BK viral load kinetics, the occurrence of AKI, and change in serum creatinine. Methods Weekly BK viral loads were obtained during the first 100 days after HCT in 403 patients between 2007-2014 (Hill et al., Blood 2017). We defined AKI according to KDIGO (Kidney Disease Improving Global Outcomes) criteria and recovery from AKI as a reduction in serum creatinine to within ten percent of baseline, both sustained for 48 hours. Viral load kinetics of interest included peak viral load, area under the curve (AUC) and cross-sectional BK viral load (log10 BK viral load). Using these weekly longitudinal measures, we estimated the relationships between BKV kinetics and AKI using generalized linear models with robust variance estimates for the outcomes of 1) mean change in serum creatinine (from baseline) and 2) odds of AKI episodes, each adjusted for acute graft versus host disease, use of nephrotoxic medications (cidofovir, foscarnet), bilirubin, conditioning regimen, age, sex, and cell source. Results Fifty-four percent (218/402) of HCT recipients had detection of BKV in at least one sample, and twenty-eight percent (113/403) had at least one BK viral load ≥ 10,000 copies/mL in the first 100 days. Sixty-eight percent (275/403) had at least one AKI episode median onset by day 27 (range 1-98). Logistic regression models did not show significant associations for log10BK viral load, peak viral load and AUC with odds of subsequent AKI (Figure1). In the linear models, BK viral load kinetics were associated with small increases in mean serum creatinine (mg/dL) by 0.025 for each log10 increase (95% CI, 0.01-0.04; p Conclusion Increased plasma BK viral load was associated with small increases in serum creatinine after allogeneic HCT, but the clinical importance of these changes is low. We found no statistically significant association between plasma BKV detection and development of AKI.