Figure 3.

Missing self specifically associates with vascular lesions (n=890 transplantations with 3476 post-transplant biopsies). (A) Association of high missing self (2–3 types) and other NK cell stimuli with kidney allograft rejection phenotypes. The estimates and 95% CIs are on the basis of a logistic mixed-effect regression model with random intercepts and a linear fixed effect of post-transplant time, corrected for HLA class I and class II mismatch number, donor age, recipient sex, and repeat transplantation. HLA-DSA positivity was defined as presence at transplantation or de novo occurrence after transplantation. The hazard ratio for cold ischemia time is given per 1-hour increase. (B) Association of high missing self with presence of individual Banff lesions, on the basis of the logistic mixed-effect regression model described in (A), with additional correction for HLA-DSA and CMV disease. OR with 95% CI are plotted. Red color indicates statistical significance. (C) Association between number of missing self types and severity of MVI in early post-transplant biopsies (n=748 biopsies). Estimates and confidence bounds are on the basis of an ordinal logistic regression model, correcting for the covariates described in (B), in addition to tacrolimus exposure and induction therapy. (D) Kaplan–Meier survival curves for incidence of transplant glomerulopathy after the first MVI biopsy, for patients without cg at diagnosis and with available histologic follow-up (n=190). Patients were stratified according to high missing self and HLA-DSA status. ABMRh, biopsies fulfilling the first 2 Banff 2019 criteria for ABMR; v, intimal arteritis; g, glomerulitis; ptc, peritubular capillaritis; i, interstitial inflammation; c4d, c4d deposition in peritubular capillaries; cg, transplant glomerulopathy; cv, arterial fibro-intimal thickening; t, tubulitis; ct, tubular atrophy; ah, arteriolar hyalinosis; ci, interstitial fibrosis.