2% and 10 3% The S-Cr level did not increase further and was sta

2% and 10.3%. The S-Cr level did not increase further and was stable at 2.8 mg/dL. The patient was discharged from our hospital on day 58. After leaving hospital, in spite of the above therapy, his S-Cr level was not decreased less than 2.7 mg/dL. The additional biopsy was performed 2 years after kidney transplantation and found the obstinate mild peritubular capillaritis and mild capillary basement membrane thickening. Further analysis showed de novo anti-DQ4 antibodies increased to 14 315 on MFI values. Again, for treatment of the

obstinate refractory AMR, we performed an additional three sessions of PEX and IVIG. In addition, we administered rituximab (200 mg/body) because his CD19/20 level increased to 1.5% and 2%. His S-Cr beta-catenin pathway level was still high at the S-Cr level

of 2.8 mg/dL 30 months after kidney transplantation. In this study, we report a refractory case of JNK inhibitor purchase PCAR accompanied by acute AMR. This case report helps to inform at least two debates: (1) the difficulties of diagnosis and management of PCAR when it is accompanied by AMR; and (2) the difficulties of diagnosis of AMR when it is resultant of anti-HLA-DQ antibody in ABO-incompatible kidney transplantation, because HLA-DQ antigen screening is not always required. PCAR is characterized by the presence of mature plasma cells that comprise more than 10% of the inflammatory cell infiltration in a renal graft.[1] This pathologic finding is noted in approximately 5–14% of patients with biopsy-proven acute rejection. Although therapy for this condition has not been generally established, graft survival is poor.[2] To diagnose PCAR, physicians should pay attention to PTLD

caused by Epstein-Barr (EB) viral infection, because the treatment for PTLD is contrary to that for PCAR.[4] In our case, we confirmed that there was no monoclonality for kappa and lambda by immunohistochemistry. In addition, EBER staining was negative by in situ hybridization. Authorities stated that there could be an AMR variant of PCAR. C4d-positive PCAR with circulating DSAbs responds adequately to treatment aimed at AMR, such as rituximab and IVIG combination of therapy. On the other hand, C4d-negative PCAR is intractable to treatment. In our case, treatment aimed at AMR showed good response. Current anti-humoral therapies in transplantation and autoimmune disease do not target the mature antibody-producing plasma cells. Matthew et al. reported that bortezomib therapy may be effective for treating mixed rejection (AMR and acute T cell-mediated rejection) with minimal toxicity and for sustaining reduction of DSAb and non-DSAb levels.[5] In this context, a strategy for treating PCAR needs to be established in the future. The importance of HLA matching in kidney transplantation is well recognized, with HLA-DR compatibility having the greatest influence on outcome.

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