#5691 BK POLYOMAVIRUS VIREMIA AND VIRURIA ARE ASSOCIATED WITH SEVERE INFLAMMATION AND FIBROSIS IN RENAL ALLOGRAFT, BUT NOT WITH GRAFT SURVIVAL

Abstract Background and Aims Infection of the renal allograft by Polyomavirus BK (BKV) causes tubular cell injury interstitial inflammation, which leads to subsequent fibrosis atrophy (IFTA). The presence degree inflammation within these areas (i-IFTA) is associated with worse outcomes in kidney transplant (KT) patients. aim this study was investigate association between BKV viremia viruria IFTA i-IFTA, decline function, graft loss. Method We conducted a single-center retrospective case-control study, included all patients who underwent an biopsy January 2018 December 2022. All biopsies were made for-cause (allograft dysfunction increased serum creatinine). Real-time polymerase chain reaction used detect quantitate viral load urine samples. Patients if they had at least 6 months since KT serial evaluation previously biopsy. evaluated, biopsy, percentage IFTA, also i-IFTA. Estimated glomerular filtration rate (eGFR) obtained baseline 1 year after Graft loss evaluated Results Mean age population 53,5 years 67% males. A total 116 performed during studied period 72 met inclusion criteria. Ten percent developed persistent (≥ 3 months) viremia, 24% viruria, 18% JCV viruria. Five cases polyomavirus-associated nephropathy diagnosed. other most common diagnoses T cell-mediated rejection (24%), antibody-mediated (15%), focal segmental glomerulosclerosis (15%). In higher strong positive i-IFTA (r=0.954; P = .001). and/or more likely present severe 40%) (grade ≥2) (P .03). degrees experience .01). There no significant eGFR, nor incidence multivariable analysis adjusted for age, eGFR time donor-specific antibodies main diagnosis predictor .04). Conclusion our population, loads extensive IFTA. independently exhibit biopsies, but dialysis shown. Longer prospective studies are needed whether infection treatment/ reduction immunosuppression can slow down progression minimizes