Abstract
Background: The prognostic role of intimal arteritis of kidney allografts in donor-specific antibody negative (DSA–) antibody-mediated rejection (ABMR) remains unclear.Methods: Seventy-two out of 881 patients who had undergone kidney transplantation from 2014 to 2017 exhibited intimal arteritis in biopsies performed during the first 12 months. In 26 DSA negative cases, the intimal arteritis was accompanied by tubulointerstitial inflammation as part of T cell-mediated vascular rejection (TCMRV, N = 26); intimal arteritis along with microvascular inflammation occurred in 29 DSA negative (ABMRV/DSA–) and 19 DSA positive cases (ABMRV, DSA+, N = 17). In 60 (83%) patients with intimal arteritis, the surveillance biopsies after antirejection therapy were performed. Hundred and two patients with non-vascular ABMR with DSA (ABMR/DSA+, N = 55) and without DSA (ABMR/DSA–, N = 47) served as controls. Time to transplant glomerulopathy (TG) and graft failure were the study endpoints.Results: Transplant glomerulopathy -free survival at 36 months was 100% in TCMRV, 85% in ABMR/DSA–, 65% in ABMRV/DSA-, 54% in ABMR/DSA+ and 31% in ABMRV/DSA+ (log rank p < 0.001). Death-censored graft survival at 36 months was 98% in ABMR/DSA-, 96% in TCMRV, 86% in ABMRV/DSA–, 79% in ABMR/DSA+, and 64% in ABMRV/DSA+ group (log rank p = 0.001). In surveillance biopsies, the resolution of rejection was found in 19 (90%) TCMRV, 14 (58%) ABMRV/DSA–, and only 4 (27%) ABMRV/DSA+ patients (p = 0.006). In the multivariable model, intimal arteritis as part of ABMR represented a significant risk for TG development (HR 2.1, 95% CI 1.2–3.8; p = 0.012) regardless of DSA status but not for graft failure at 36 months.Conclusions: Intimal arteritis as part of ABMR represented a risk for early development of TG regardless of the presence or absence of DSA. Intimal arteritis in DSA positive ABMR represented the high-risk phenotype.
Highlights
Antibody-mediated rejection (ABMR) represents a major obstacle in achieving long-term graft function and survival [1]
Lefaucheur et al revealed a detrimental impact of intimal arteritis associated with donorspecific antibodies (DSA) on graft prognosis exceeding other rejection phenotypes, and any grade of intimal arteritis has been included in the Banff classification as a histologic feature of ABMR [6]
DSA– phenotypes were more common after the first transplantation
Summary
Antibody-mediated rejection (ABMR) represents a major obstacle in achieving long-term graft function and survival [1]. I.e., v-lesion defined by Banff histological criteria, is a morphologic feature of vascular rejection. It represents a diagnostic and therapeutic challenge as it is involved in histologic criteria of both T cell-mediated rejection (TCMR) and ABMR [2]. Previously intimal arteritis was recognized as the rejection phenotype often resistant to steroid treatment [4], more recently, the association of intimal arteritis with DSA was described [5]. Lefaucheur et al revealed a detrimental impact of intimal arteritis associated with DSA on graft prognosis exceeding other rejection phenotypes, and any grade of intimal arteritis has been included in the Banff classification as a histologic feature of ABMR [6]. The prognostic role of intimal arteritis of kidney allografts in donor-specific antibody negative (DSA–) antibody-mediated rejection (ABMR) remains unclear
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