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The Severity of Acute Cellular Rejection Defined by Banff Classification Is Associated With Kidney Allograft Outcomes

Wu, Kaiyin1; Budde, Klemens1; Lu, Huber1; Schmidt, Danilo1; Liefeldt, Lutz1; Glander, Petra1; Neumayer, Hans Helmut1; Rudolph, Birgit2,3

doi: 10.1097/01.TP.0000441094.32217.05
Clinical and Translational Research

Background: It is unclear if the severity or the timing of acute cellular rejection (ACR) defined by Banff classification 2009 is associated with graft survival.

Methods: Borderline changes, TCMR I (interstitial rejection), and TCMR II/III (vascular rejection) were defined as low, moderate, and high ACR severity, respectively. Approximately 270 patients who had at least one episode of ACR were enrolled, 270 biopsies were chosen which showed the highest ACR severity of each patient and were negative for donor-specific antibodies (DSA), C4d, and microcirculation changes (MC). Six months were used as the cutoff to define early and late ACR; 370 patients without biopsy posttransplantation were recruited in the control group.

Results: Up to 8-year posttransplantation, death-censored graft survival (DCGS) rates of control, borderline, TCMR I, and TCMR II/III groups were 97.6%, 93.3%, 79.6%, and 73.6% (log rank test, P<0.001); the control group had significantly higher DCGS rate than the three ACR groups (each pairwise comparison yields P<0.05). The DCGS rate of late ACR was significantly lower compared with early ACR (63.6% vs. 87.4%, P<0.001). Intimal arteritis (Banff v-lesion) was an independent histologic risk factor correlated with long-term graft loss regardless of the timing of ACR. The v-lesions with minimal or high-grade tubulitis displayed similar graft survival (72.7% vs. 72.9%, P=0.96).

Conclusion: All types of ACR affect long-term graft survival. Vascular or late ACR predict poorer graft survival; the extent of tubulointerstitial inflammation (TI) is of no prognostic significance for vascular rejection.

1 Medizinische Klinik mit Schwerpunkt Nephrologie, Charité Campus Mitte, Universitätsmedizin Berlin, Germany.

2 Institut für Pathologie, Charité Campus Mitte, Universitätsmedizin Berlin, Germany.

3 Address correspondence to: Dr. Birgit Rudolph, Institut für Pathologie, Charite Campus Mitte, Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.

Partial data of this study have been presented at the 24th International Congress of the Transplantation Society.

The authors declare no funding or conflicts of interest.

E-mail: Birgit.rudolph@charite.de

K.W. participated in the performance of the research and writing the paper. K.B. and H.H.N. participated in the research design. L.H. participated in processing data and writing the paper. D.S. participated in data administration. L.L. participated in clinical work of this research. P.G. participated in laboratory work of this research. B.R. participated in evaluation of pathologic slices, research design, and writing.

Received 25 March 2013. Revision requested 4 April 2013.

Accepted 11 November 2013.

© 2014 by Lippincott Williams & Wilkins