A case of plasmacytic hyperplasia arising in a kidney allograft salvaged with immunosuppression reduction alone

Abstract

Post-transplant lymphoproliferative disorder (PTLD) is a well-known complication of organ transplantation. Plasmacytic hyperplasia (PH) is thought of as the mildest form of PTLD; however, a graftectomy is necessary in most situations. We experienced an interesting case of PH arising in a kidney allograft, which could be relieved with a reduction in immunosuppression. A 27-year-old female underwent a living-related kidney transplantation. A 3-month non-episode protocol biopsy unexpectedly showed the devastating appearance of polymorphic plasma cell infiltration into the graft intersitium, compatible with PH. The PH was located in the graft by radiographic examinations. The infiltration of plasma cell disappeared completely on the 6-month graft biopsy specimen following immunosuppression reduction and the graft is functioning, although it was damaged by a subsequent acute rejection. Our present case indicates that some PTLD can be completely cured with a reduction in immunosuppression alone. The diagnostic modality for the evaluation of PTLD cell extinction is necessary to maintain graft function with adequate immunosuppression thereafter.

Renal graft loss with plasma cell‐rich acute rejection in cadaveric renal transplantation: a case report

“…Harada et al. (7) have reported a case of PH or an early lesion of PTLD treated by reducing immunosuppression. Scattered plasma cells and plasmacytoid lymphocytes and immunoblasts were seen in the interstitium; they reduced immunosuppression, and the two series of allograft biopsies that followed revealed partial and then complete regression of PTLD.…”

Array CGH-based analysis of post-transplant plasmacytic hyperplasia reveals ‘intact genomes’ arguing against categorizing it as part of the post-transplant lymphoproliferative disease spectrum

“…In 2007, Vakiani et al [3] proposed a third entity of ePTLD described as follicular hyperplasia, which showed cytogenetic abnormalities using Giemsa banding and spectral karyotype analysis. Most ePTLD arise in the adenoids or lymph nodes; however, there are also rare case reports on ePTLD arising in the transplanted organs as well [4]. The absence of clonality does not exclude malignancy and cytogenetic abnormalities have been documented in ePTLD previously [3].…”