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Histological Evolution of BK Virus–Associated Nephropathy: Importance of Integrating Clinical and Pathological Findings
Author(s) -
Drachenberg C. B.,
Papadimitriou J. C.,
Chaudhry M. R.,
Ugarte R.,
Mavanur M.,
Thomas B.,
Cangro C.,
Costa N.,
Ramos E.,
Weir M. R.,
Haririan A.
Publication year - 2017
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.14314
Subject(s) - medicine , immunosuppression , biopsy , viremia , polyomavirus infections , nephropathy , bk virus , pathological , pathology , viral load , transplantation , immunology , gastroenterology , kidney transplantation , antibody , virus , diabetes mellitus , endocrinology
Long‐term clinicopathological studies of BK ‐associated nephropathy (Py VAN ) are not available. We studied 206 biopsies (71 patients), followed 3.09 ± 1.46 years after immunosuppression reduction. The biopsy features (% immunostain for PyV large T ag + staining and inflammation ± acute rejection) were correlated with viral load dynamics and serum creatinine to define the clinicopathological status (Py VCPS ). Incidence of acute rejection was 28% in the second biopsy and 50% subsequently (25% mixed T cell–mediated allograft rejection (TCMR) + antibody‐mediated allograft rejection (AMR); rejection overall affected 38% of patients (>50% AMR ). Graft loss was 15.4% (0.8–5.3 years after Py VAN ); 76% had complete viral clearance (mean 28 weeks). The only predictors of graft loss were acute rejection ( TCMR p = 0.008, any type p = 0.07), and increased “t” and “ci” in the second biopsy (p = 0.006 and 0.048). Higher peak viremia correlated with poorer viral clearance (p = 0.002). Presumptive and proven Py VAN had similar presentation, evolution, and outcome. Late Py VAN (>2 years, 9.8%) justifies BK viremia evaluation at any point with graft dysfunction and/or biopsy evaluation. This study describes the histological evolution of Py VAN and corresponding clinicopathological correlations. Although the pathological features overall reflect the viral and immunological interactions, the Py VAN course remains difficult to predict based on any single feature. Appropriate clinical management requires repeat biopsies and determination of the Py VCPS at relevant time points, for corresponding personalized immunosuppression adjustment.