POS-716 SUSTAINED BK VIRURIA: A FORGOTTEN ALLY FOR EARLY DIAGNOSIS OF BK VIRUS NEPHROPATHY IN KIDNEY TRANSPLANTATION

Abstract

BK virus nephropathy (BKVN) is a major complication of kidney transplant (KT). Usually, the sequence of the disease is described as an asymptomatic period of viruria, followed by viremia and subsequently, by BKVN. The association of BKVN with viruria but without viremia, is infrequently described. Retrospective study of KT patients with biopsy proven BKVN, from January of 2011 to October of 2020, with viruria but no viremia. Of the 574 KT performed at our center during the study period, 16 patients (2,8%) had biopsy proven BKVN. 4 patients met the inclusion criteria.Patient 1: A 59-years-old man underwent a 3 antigen (Atg) mismatch (MM) brain dead donor KT. Immunosuppression (IS) consisted of Basiliximab, Tacrolimus (TAC), Mycophenolate Mofetil (MMF) and Prednisolone (PDN). KT was complicated by delayed graft function (DGF). He had no acute rejection (AR) nor donor specific antibodies (DSA). 19,3 months after KT he had CMV infection treated with Ganciclovir and suspension of MMF. 1 month later, BK viruria appeared (7,7 log copies/mL with a maximum of >9 log copies/mL) without viremia nor kidney dysfunction. Later because of kidney disfunction and persistent viruria he did a KT biopsy, showing a BKVN pattern B1 according to AST classification. IS was changed to everolimus (EVR) and low dose TAC. He evolved favourably, returning to baseline serum creatinine and clearance of BK viruria.Patient 2: A 52-years-old female underwent 2 Atg MM circulatory dead donor (CDD) KT. IS consisted of anti-thymocyte globulin (ATG), TAC, MMF and PDN. KT was complicated by DGF, without AR nor DSA. Baseline Screat was 1,3 mg/dL. Nine months after KT, she developed BK viruria (5,2log copies/mL) without viremia. Because of persistent viruria and allograft disfunction a KT biopsy was performed showing BKVN (Pattern A). MMF was suspended and TAC was reduced, without clinical nor virologic improvement and IS was switched to EVR and low dose TAC, without response and a repeated KT biopsy revealed a BKVN pattern C, with no further therapeutic interventions. Patient 3: A 48-years-old female underwent 5 Atg MM CDD KT. IS consisted of ATG, TAC, MMF and PDN. She had no DGF nor AR or DSA and baseline Screat was 0,8-0,9 mg/dL. Nine months after KT, BK viruria appeared (4log copies/mL) and MMF was reduced. Persistent viruria without BK viraemia and kidney dysfunction led to a KT biopsy which showed BKVN (patternC). IS was changed to EVR and low dose TAC with no response.Patient 4: An HIV-1 positive, 26 years-old man underwent a 5 Atg MM CDD KT. IS consisted of ATG, TAC, MMF and PDN. CD4+ T cell numbers 3 months after KT were 781 cells/mm3. Baseline Screat was 1,5mg/dL. One month after KT, he had BK viruria (8log copies/mL), without BK viremia, and 9 months latter his Screat increased to 1.9 mg/dL, with persistent BK viruria without viremia. A KT biopsy was done with positivity for SV40 but without enough tissue representation to classify the BK pattern. MMF dose was reduced, and on last follow-up Screat was 1.9mg/dl. MMF was suspended. Screening for BK virus remains uncertain. Our study highlights the importance of BK viruria screening, and that BKVN should be considered in KT patients with allograft disfunction and persistent viruria, even without viremia. The early recognition of BK viruria could guide early therapeutic decisions with impact on the outcome of BKVN.