A case of second renal transplantation with acute antibody‐mediated rejection complicated with BK virus nephropathy

Abstract

Atsumi H, Asaka M, Kimura S, Imura J, Fujimoto K, Chikazawa Y, Nakagawa M, Okuyama H, Yamaya H, Moriyama M, Tanaka T, Suzuki K, Yokoyama H. A case of second renal transplantation with acute antibody‐mediated rejection complicated with BK virus nephropathy. Clin Transplant 2010: 24 (Suppl. 22): 35–38. © 2010 John Wiley & Sons A/S. Abstract: We reported a 40‐year‐old female case of second renal transplantation with antibody‐mediated rejection (AMR) complicated by BK virus nephropathy. She started hemodialysis (HD) at the age of 17 because of IgA nephropathy. At the age of 18, she underwent living‐donor kidney transplantation from her father, but two and a half years after transplantation, she developed chronic rejection. This time, she received cadaveric renal transplantation under the negative cross‐match (AHG‐LCT), and HLA‐AB 1 mismatch and ‐DR 1 mismatch. Immunosuppressive therapy was initiated using the following four immunosuppressants: methylprednisolone, mycophenolate mofetil, cyclosporine, and basiliximab. However, renal graft showed delayed function, the biopsy showed glomerulitis (g2), endarteritis (v1), and cellular infiltration (ptc3) consisting mainly of mononuclear cells in the peritubular capillary with diffusely positive C4d and anti‐SV 40 large T‐antigen‐positive renal tubular epithelial cells on post‐operative day 19. The donor‐specific antibody for HLA‐B46 was proven by the LAB screen method. We performed plasma exchange three times and administered immunoglobulin (15 g in total). Then, methylprednisolone pulse therapy was added, and the serum creatinine (SCr) levels gradually decreased. On post‐operative day 44, the patient was removed from HD and was discharged with SCr level of 3.3 mg/dL.

In kidney transplant recipients with BK polyomavirus infection, early BK nephropathy, microvascular inflammation, and serum creatinine are risk factors for graft loss

“…These observations are supported by previous case reports and series that examined concomitant C4d and BK staining in renal transplant recipients (21,22,28). Honsova et al (28) reported BKVN and focally positive C4d in 9/12 needle biopsy samples and 2 nephrectomy samples and noted that the ptc vascular endothelium posed a potential target for antibody response after injury from BKPyV infection.…”

Pathology of Resolving Polyomavirus-Associated Nephropathy

“…The appearance of IEL and interstitial inflammation are not specific for resolving PyVAN, and in our opinion the distinction of concurrent ICR is currently impossible. The main arguments for resolving PyVAN in our cohort are (1) PyVAN and acute rejection may not be mutually exclusive as concurrent vascular and/or antibody-mediated rejection has been reported in the literature in humans (28)(29)(30)(31)(32) as well as in a mouse models of BKV (33). It is interesting to note that patients with BKV viruria in the absence of viremia have a mild increase in the number of putative episodes of T-cell-mediated rejection (34,35).…”

“…The main arguments for resolving PyVAN in our cohort are (1) PyVAN and acute rejection may not be mutually exclusive as concurrent vascular and/or antibody-mediated rejection has been reported in the literature in humans (28)(29)(30)(31)(32) as well as in a mouse models of BKV (33). The main arguments for resolving PyVAN in our cohort are (1) PyVAN and acute rejection may not be mutually exclusive as concurrent vascular and/or antibody-mediated rejection has been reported in the literature in humans (28)(29)(30)(31)(32) as well as in a mouse models of BKV (33).…”

Pathology of Resolving Polyomavirus-Associated Nephropathy

“…PyVAN and acute rejection may not be mutually exclusive as concurrent vascular and/or antibody‐mediated rejection has been reported in the literature in humans as well as in a mouse models of BKV . It is interesting to note that patients with BKV viruria in the absence of viremia have a mild increase in the number of putative episodes of T‐cell‐mediated rejection .…”