ABSTRACT:We report a case of plasma cell-rich rejection accompanied by acute antibody-mediated rejection in a patient with ABO-incompatible kidney transplantation. A 33-year-old man was admitted for an episode biopsy; he had a serum creatinine (S-Cr) level of 5.7 mg/dL 1 year following primary kidney transplantation. Histological features included two distinct entities: (1) a focal, aggressive tubulointerstitial inflammatory cell (predominantly plasma cells) infiltration with moderate tubulitis; and (2) inflammatory cell infiltration (including neutrophils) in peritubular capillaries. Substantial laboratory examination showed that the patient had donor-specific antibodies for DQ4 and DQ6. Considering both the histological and laboratory findings, we diagnosed him with plasma cell-rich rejection accompanied by acute antibody-mediated rejection. We started 3 days of consecutive steroid pulse therapy three times every 2 weeks for the former and plasma exchange with intravenous immunoglobulin (IVIG) for the latter histological feature. One month after treatment, a second allograft biopsy showed excellent responses to treatment for plasma cell-rich rejection, but moderate, acute antibody-mediated rejection remained. Therefore, we added plasma exchange with IVIG again. After treatment, allograft function was stable, with an S-Cr level of 2.8 mg/dL. This case report demonstrates the difficulty of the diagnosis of, and treatment for, plasma cell-rich rejection accompanied by acute antibody-mediated rejection in a patient with ABOincompatible kidney transplantation. We also include a review of the related literature.Both plasma cell-rich rejection (PCAR) and acute antibodymediated rejection (AMR) remain refractory rejection entities in spite of the recent development and establishment of immunosuppressive therapy. The former is characterized by the presence of mature plasma cells that comprise more than 10% of the inflammatory cell infiltration in a renal allograft.1 PCAR is a rare type of rejection noted in approximately 5-14% of patients with biopsy-proven acute rejection, but graft survival is poor and standard therapeutic options have yet to be generally established.2 The latter is a well-recognized type of rejection that is due in large part to antibodies to human leukocyte antigen (HLA) alleles. Recent studies have focused on not only HLA-DR compatibility, but also on that of HLA-DQ, since de novo DQ donor-specific antibodies (DSAbs) are the predominant HLA class II DSAbs found after transplantation. 3 We report here a refractory case of PCAR accompanied by AMR due to de novo DQ DSAbs 1 year after ABOincompatible, living-related kidney transplantation. CASE REPORTA 33-year-old Japanese man was admitted to our hospital for an episode biopsy 1 year following primary kidney transplantation. He was diagnosed with IgA nephropathy at the age of 31 years and received a living-related kidney transplantation at the age of 32 from his mother. ABO blood types were incompatible, and HLA alleles were mismatched at two bs_bs_ban...

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Background Previous studies have shown that a donor/recipient body weight mismatch affects long‐term graft survival and graft function after kidney transplantation. However, the mechanisms are not fully understood. Aim To address the mechanisms, we compared the pathological and physiological features between patients with a donor/recipient body weight mismatch and those without a mismatch 1 yr after kidney transplantation. Furthermore, we investigated the correlation with the donor/recipient body weight ratio. Methods We examined allograft biopsy specimens from 10 recipients with stable kidney function, with body weight mismatch (donor/recipient body weight ratio [D/R BWR] < 0.9), and compared them with samples from 13 patients without mismatch. We measured glomerular volume (GV) using the Weibel–Gomez method and glomerular density (GD) defined by nonsclerotic glomerular number/renal cortical area as pathological findings. The physiological parameters included estimated glomerular filtration rate and proteinuria (mg/day). These data were evaluated to identify a correlation with D/R BWR. Results The pathological features showed that GV and GD were identical in the two groups. However, when glomerular enlargement was defined by ΔGV (GV at the 1‐yr biopsy minus GV at baseline biopsy), ΔGV was higher in mismatch cases compared with that in cases without a mismatch (10.6 ± 4.6 vs. 5.5 ± 7.1 × 105 μm3; P = 0.049). Furthermore, D/R BWR was significantly correlated with ΔGV (P = 0.03, r = –0.436). eGFR values were physiologically identical between the two groups, but the mismatch cases had significantly higher proteinuria levels than that of the cases without a mismatch at 1 yr after kidney transplantation. Conclusion A donor/recipient body weight mismatch could affect glomerular enlargement and increased proteinuria 1 yr after kidney transplantation. How these two features affect long‐term graft survival and function must be addressed in the future.

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