Plasma cell-rich acute rejection (PCAR) is a rare type of allograft rejection characterized by the presence of mature plasma cells. In general, the prognosis of PCAR is poor, and its clinical and pathological features remain unclear.
We performed a retrospective observational study and compared allograft survival between kidney transplant recipients who developed PCAR and those who did not develop PCAR. We further analyzed clinical and pathological risk factors for allograft failure in PCAR patients.
Of 1956 recipients, 40 developed PCAR. There was a higher prevalence of deceased donor transplants (27.5% vs 11.7%, P = 0.0059), longer median total ischemia time (99 minutes; interquartile range, 71-144 vs 77 minutes; interquartile range, 59-111; P = 0.0309), and lower prevalence of ABO-incompatible transplantation (7.5% vs 22.5%; P = 0.0206) in patients with PCAR than in those without PCAR.
Multivariate Cox regression analysis showed that development of PCAR was associated with allograft loss (hazard ratio, 8.03; 95% confidence interval, 3.89-14.80; P < 0.0001).
We classified PCAR according to the Banff 2015 criteria into a borderline change group, a T cell–mediated rejection (TCMR) group, an antibody-mediated rejection (AMR) or suspected of having AMR (AMR/sAMR) group, and a mixed rejection (TCMR/AMR) group. The AMR/sAMR group was associated with a lower rate of allograft survival without significant difference (log-rank test, P = 0.1692).
The results indicated that PCAR was an independent risk factor for allograft loss. PCAR presented with all types of rejection in the Banff 2015 criteria, and AMR/sAMR was associated with poor allograft survival.
Plasma cell-rich acute rejection is a rare and ill-defined category of acute rejection encountered in kidney transplant recipients. In this small series, the authors improve out knowledge regarding both clinical presentation and prognosis.
1 Department of Urology, Tokyo Women’s Medical University, Kawadacho, Shinjuku-ku, Tokyo, Japan.
2 Department of Nephrology, Tokyo Metropolitan Health and Medical Treatment Corporation Okubo Hospital, Kabukicho, Shinjuku-ku, Tokyo, Japan.
3 Department of Anatomy, Showa School of Medicine, Hatanodai, Shinagawa-ku, Tokyo, Japan.
4 Department of Urology, Tokyo Metropolitan Health and Medical Treatment Corporation Okubo Hospital, Kabukicho, Shinjuku-ku, Tokyo, Japan.
5 Department of Surgery, Tokyo Women’s Medical University, Kawadacho, Shinjuku-ku, Tokyo, Japan.
6 Department of Pediatric Nephrology, Tokyo Women’s Medical University, Kawadacho, Shinjuku-ku, Tokyo, Japan.
Received 14 June 2017. Revision received 18 October 2017.
Accepted 19 October 2017.
The authors declare no funding or conflicts of interest.
J.H. and K.H. participated in study design. J.H., H.S., K.O., M.O., S.F., and M.H. participated in collecting the data. J.H., K.H., and M.O. participated in the data analysis and interpretation. J.H., K.H., and M.O. participated in statistical analysis. J.H., K.H., K.O., and M.O. participated in writing the article. S.W., H.S., H.I., S.F., M.H., and K.T. participated in the performance of the study and provided significant intellectual input.
Correspondence: Kazunari Tanabe, MD, PhD, Department of Urology, Tokyo Women’s Medical University, 8-1, Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan. (firstname.lastname@example.org).