Plasma cell-rich acute rejection after renal transplantation in a patient with pyoderma gangrenosum: a case report.

A 40-yr-old female received a living-related renal transplantation on January 29, 2008. She had type I diabetes mellitus and pyoderma gangrenosum (PG). Induction immunosuppressive therapy consisted of tacrolimus, mycophenolate mofetil, basiliximab, and prednisolone. Intravenous methylprednisolone pulse therapy was administered to prevent ulceration at the surgical site. The postoperative outcome was almost uneventful, and renal graft function was well preserved for 11 months. Her graft function deteriorated on December 24, 2008 and thus an episode biopsy was performed. The histopathological findings were consistent with plasma cell-rich acute rejection (PCAR). During hospitalization, it was noted that the patient was non-compliant. We then performed steroid pulse therapy, and her graft function and histological findings improved. This is the first report of PCAR in a patient with PG who received a renal allograft. It was thought that PCAR was triggered because of her non-compliance. Thus, we should recognize the importance of enhancing compliance in transplant recipients.

Does MICA influence acute rejection in kidney transplantation?

MHC class 1-related chain A (MICA) has been reported to be recognized by specific antibodies in the sera of transplanted patients, and it may be a target molecule in allograft rejection. MICA was originally pointed out to be an HLA-related polymorphic gene, the product of which may be recognized by a subpopulation of intestinal gamma delta T-cells and may play a role in the activation of a subpopulation of natural killer cells. Although their association with chronic rejection has been demonstrated before, there are few reports of any relation with acute rejection. We encountered a possible case of MICA-related acute early rejection. The recipient was a 25-year-old female; the original disease was IgA nephropathy, and the hemodialysis period was 12 months. She underwent ABO-compatible living-related renal transplantation from her mother. The HLA type was A24, A31, B7, B52, DR1, and DR15 in the donor and A31, A33, B7, B44, DR1, and DR12 in the recipient. A pre-operative direct cross-match was negative by a conventional cytotoxic test, and HLA class 1 and 2 antibodies were negative by LABScreen single antigen testing. Induction immunosuppressive therapy was started with TAC, MMF, MP, and BXM. The graft functioned at once, and SCr was 2.4 mg/dl on post-transplant day 1. SCr increased from post-transplant day 2, and oliguria progressed. Hemodialysis was restarted on post-transplant day 6. A biopsy revealed Banff 2b vascular rejection. The graft was finally rescued by steroid pulse and plasma exchange therapy. SCr went down to 1.07 mg/dl, and a re-biopsy showed improvement on post-transplant day 42. HLA class 1 and 2 antibodies were negative during this period, and MICA019 antibody was higher before transplantation retrospectively. Additionally, this antibody titer was decreased at the time of discharge. These data show that MICA may induce rejection in the early phase of renal transplantation. Further study is needed to evaluate this phenomenon.