Clinicopathological features and outcomes of kidney allografts in plasma cell‐rich acute rejection: A case series

Abstract

Plasma cell-rich acute rejection (PCAR) is a rare type of acute rejection in renal transplantation. Despite aggressive immunotherapy, approximately 40-60% of patients develop graft loss within 1 year after an episode of PCAR. However, the reason for this outcome remains obscure. This study retrospectively identified six patients with PCAR diagnosed between 2009 and 2015 at a single university hospital. Clinicopathological data were collected. Five of the six patients were male, and mean age at the onset of PCAR was 49.0 ±14.5 years. None of the patients showed overall poor adherence to medication. Mean time to diagnosis was 302 ±234 days post-transplantation. All patients had preceding or concurrent viral infection. Four patients developed PCAR alone and two patients developed PCAR with antibody-mediated rejection. One of the six patients showed both severe tubulointerstitial and microvascular inflammation (total of Banff tubulitis 't' + interstitial inflammation 'i' + glomerulitis 'g' + peritubular capillaritis 'ptc' scores >10). This patient had progressive worsening of graft function and re-initiated dialysis at 74 months after a PCAR episode. In addition, three of the six patients had long-term recurrence of PCAR. With the recurrence of PCAR, patients with both moderate tubulointerstitial and microvascular inflammation (total of Banff 't' + 'i' + 'g' + 'ptc' scores >6) had progressive worsening of graft function. In summary, the present results suggest that concurrent moderate to severe tubulointerstitial and microvascular inflammation may lead to poor outcomes of graft function after a PCAR episode.

B Cell Activating Factor (BAFF) Is Required for the Development of Intra-Renal Tertiary Lymphoid Organs in Experimental Kidney Transplantation in Rats

“…We investigated the presence of plasma cells within allografts in our model. Although the exact effector function of intra-renal plasma cells and their role in allograft rejection is not fully understood, intra-renal plasma cells have been associated with chronic allograft rejection and poor prognosis [24,[33][34][35][36]. Although we have previously shown that anti-BAFF therapy reduced the number of splenic plasma cells [23], the difference in intra-renal plasma cells between groups was not statistically significant in this study.…”

Late Onset Graft Plasmacytoma-Like PTLD Presenting as Acute Hyperglycemia in a Kidney-Pancreas Transplant Recipient

“…In our case, single antigen assay was not performed, but solid-phase single bead Luminex® screening was negative the day of pancreas biopsy, being therefore unlikely to present a donor-specific antibody (DSA). Recently, Hamada et al described a case series of kidney transplant recipients with plasma cell rich acute rejection (PCAR) [21]. Of the 6 patients, only two were characterized as presenting an acute rejection, and all the remaining four cases did not present DSAs.…”

Clinicopathological and Molecular Characteristics of Plasma Cell Rich Rejection in Renal Transplant Biopsies

“…Histologically, PCRR is characterized by the presence of plasma cells, either diffusely distributed in the renal tissue or aggregated into clusters, often accompanied by myxoid interstitial edema, with variable degrees of tubulitis, arteritis, microvascular inflammation and often capillary C4d deposition with or without donor-specific antibodies. [2][3][4] In general, PCRR manifests at a later time post-transplant than TCMR, ranging from 302 days to 3.7 years post-transplant according to current literature. [3][4][5][6][7] The majority of patients with PCRR present with histopathological patterns similar to TMCR type I or II.…”

“…Histologically, PCRR is characterized by the presence of plasma cells, either diffusely distributed in the renal tissue or aggregated into clusters, often accompanied by myxoid interstitial edema, with variable degrees of tubulitis, arteritis, microvascular inflammation and often capillary C4d deposition with or without donor-specific antibodies. 2–4…”