Kidney Allograft Outcomes in Borderline and T Cell-Mediated Rejection With Microvascular Inflammation

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Introduction: Microvascular inflammation (MVI) is a hallmark feature of antibody-mediated rejection (ABMR), but its prognostic significance when it occurs with T-cell-mediated rejection (TCMR) in the absence of other ABMR features remains unclear. Methods: We examined the association between pure TCMR phenotypes, defined by the presence or absence of MVI, and graft survival using restricted mean survival time (RMST), and assessed interactions with rejection involving a "v" lesion. Results: Among 1614 recipients with first biopsy-proven pure TCMR (2010-2023), 85% had no MVI, 8% subthreshold MVI (Banff glomerulitis [g] + peritubular capillaritis [ptc] = 1), and 7% with MVI (g + ptc ≥ 2). Compared with TCMR without MVI, recipients with TCMR + MVI (hazard ratio [HR]; 95% confidence intervals [CI] 1.57 [1.06-2.34]) had a higher risk of all-cause graft loss, whereas subthreshold MVI was not associated with increased risk. The 5-year RMST was lowest in the MVI group (3.93 [3.53-4.26]), compared with the subthreshold group (4.39 [4.11- 4.60]) and the no MVI group (4.32 [4.24-4.40]). Rejection with a "v" lesion modified this association. Recipients with TCMR + MVI and positive "v" lesion had a 2.77-fold higher risk of graft loss (2.77 [1.64-4.67]), whereas no excess risk was observed in those without vascular lesions. Conclusion: Pure TCMR with MVI, particularly in the setting of a "v" lesion, represents a high-risk phenotype associated with poorer graft survival, warranting mechanistic investigations and targeted therapeutic strategies.

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