TY - JOUR
T1 - Treatment of chronic active T cell-mediated rejection after kidney transplantation
T2 - A retrospective cohort study of 37 transplants
AU - Noguchi, Hiroshi
AU - Matsukuma, Yuta
AU - Nakagawa, Kaneyasu
AU - Ueki, Kenji
AU - tsuchimoto, akihiro
AU - Nakano, Toshiaki
AU - Sato, Yu
AU - Kaku, Keizo
AU - Okabe, Yasuhiro
AU - Nakamura, Masafumi
N1 - Funding Information:
The authors would like to thank Ms. Yasuka Ogawa for her assistance with the data collection. We also thank Jane Charbonneau, DVM, and H. Nikki March, PhD, from Edanz (https://jp.edanz.com/ac) for editing drafts of this manuscript.
Publisher Copyright:
© 2022 Asian Pacific Society of Nephrology.
PY - 2022/7
Y1 - 2022/7
N2 - Aim: Data on the treatment of chronic active T cell-mediated rejection (CA-TCMR) are scarce, and therapeutical strategies for CA-TCMR have not been established. We retrospectively evaluated the outcomes and effects of treatment on pathological and clinical findings in patients with CA-TCMR. Methods: This study comprised 37 patients who underwent kidney transplantation at our institute who were diagnosed with CA-TCMR between January 2018 and December 2020. Patients were followed until October 2021. Results: A total of 32 of the 37 patients were treated. During the observation period, two patients died (5%), and five patients developed allograft loss (13%). A univariate Cox proportional hazards model showed that indication biopsy, higher spot urine protein/creatinine ratio (UPCR) and Banff ci/ct scores were risk factors for allograft loss. Of the treated patients, 23 underwent follow-up biopsies. The Wilcoxon signed-rank test showed significant improvement in the Baff scores for “ti”, “i-IFTA”, “t” and “t-IFTA” after treatment. On pathology, 13 (57%) of the patients who underwent follow-up biopsy improved to “no evidence of rejection” or “borderline change.” Assuming that improvement in pathology to “borderline change” or “no evidence of rejection” on follow-up biopsy indicates response to treatment, multivariate logistic analysis showed that lower UPCR was a predictive factor for response to treatment. No specific effect of treatment type was observed. Conclusions: Our results indicate that treatment could improve the pathological findings in CA-TCMR.
AB - Aim: Data on the treatment of chronic active T cell-mediated rejection (CA-TCMR) are scarce, and therapeutical strategies for CA-TCMR have not been established. We retrospectively evaluated the outcomes and effects of treatment on pathological and clinical findings in patients with CA-TCMR. Methods: This study comprised 37 patients who underwent kidney transplantation at our institute who were diagnosed with CA-TCMR between January 2018 and December 2020. Patients were followed until October 2021. Results: A total of 32 of the 37 patients were treated. During the observation period, two patients died (5%), and five patients developed allograft loss (13%). A univariate Cox proportional hazards model showed that indication biopsy, higher spot urine protein/creatinine ratio (UPCR) and Banff ci/ct scores were risk factors for allograft loss. Of the treated patients, 23 underwent follow-up biopsies. The Wilcoxon signed-rank test showed significant improvement in the Baff scores for “ti”, “i-IFTA”, “t” and “t-IFTA” after treatment. On pathology, 13 (57%) of the patients who underwent follow-up biopsy improved to “no evidence of rejection” or “borderline change.” Assuming that improvement in pathology to “borderline change” or “no evidence of rejection” on follow-up biopsy indicates response to treatment, multivariate logistic analysis showed that lower UPCR was a predictive factor for response to treatment. No specific effect of treatment type was observed. Conclusions: Our results indicate that treatment could improve the pathological findings in CA-TCMR.
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U2 - 10.1111/nep.14048
DO - 10.1111/nep.14048
M3 - Article
C2 - 35478476
AN - SCOPUS:85129154108
SN - 1320-5358
VL - 27
SP - 632
EP - 638
JO - Nephrology
JF - Nephrology
IS - 7
ER -