TABLE 4.
Multivariable Cox model of the composite endpoint
| Parameter | Univariable HR (95% CI) | P | Multivariable HR (95% CI) | P |
|---|---|---|---|---|
| Subclinical inflammation (vs no major abnormalities) | 4.15 (1.85-9.32) | 0.001 | 2.88 (1.11-7.51) | 0.03 |
| SC-B-TCMR (i0t1 threshold) | 3.15 (1.21-8.16) | 0.02 | 2.39 (0.82-6.95) | 0.11 |
| SC-B-TCMR (i1t1 threshold) | 7.01 (2.34-20.94) | 0.0005 | 5.32 (1.37-20.7) | 0.02 |
| SC-TCMR | — | — | — | — |
| SC-MVI | 9.41 (2.87-30.85) | 0.0002 | 3.18 (0.73-13.83) | 0.12 |
| ti score (0–3) | 1.96 (1.17-3.29) | 0.01 | 1.18 (0.52-2.71) | 0.69 |
| ci score (0–3) | 1.54 (0.82-2.92) | 0.18 | ||
| ct score (0–3) | 1.94 (0.87-4.29) | 0.11 | ||
| cg score (0–3) | 4.08 (1.23-13.62) | 0.02 | 3.93 (0.98-15.72) | 0.05 |
| cv score (0–3) | 1.62 (1.06-2.47) | 0.03 | 1.28 (0.77-2.12) | 0.35 |
| Age at transplant (per year) | 0.99 (0.95-1.02) | 0.37 | ||
| Black race (vs non-Black race) | 1.69 (0.72-4.00) | 0.23 | ||
| Deceased donor (vs living donor) | 2.51 (0.93-6.75) | 0.07 | 2.24 (0.83-6.05) | 0.11 |
| Male sex (vs female sex) | 0.68 (0.30-1.54) | 0.36 | ||
| Pretransplant diabetes mellitus (vs no diabetes) | 0.89 (0.37-2.17) | 0.80 | ||
| Repeat transplant (vs first transplant) | 0.74 (0.17-3.17) | 0.69 | ||
| DSA at surveillance (vs no DSA) | 2.10 (0.62-7.07) | 0.23 | ||
| Estimated GFR (per 1 mL/min/1.73 m2) | 0.99 (0.97-1.01) | 0.52 | ||
| Urine protein-to-creatinine ratio at surveillance (per unit) | 7.74 (3.05-19.61) | <0.0001 | 4.85 (1.53-15.35) | 0.007 |
Multivariable Cox proportional hazards model of a composite endpoint of acute rejection after surveillance, death-censored allograft failure, and death with a functioning allograft. We tested the association between subclinical inflammation phenotypes (with SC-B-TCMR defined using the Banff 2017 i0t1 threshold as well as the Banff 2019 i1t1 threshold), individual Banff chronic injury scores, and clinical covariates with the composite endpoint in univariable models. We excluded Banff acute injury scores (except for ti) because of collinearity with subclinical inflammation phenotypes. All covariates that were significantly associated with the composite endpoint at P < 0.10 by univariable modeling were force entered into a multivariable Cox model. There were no outcome events in the SC-TCMR phenotype (reflected as “—“ in the table). The final Cox model was significant at P < 0.0001, df 9, and chi-square 50.98.
cg, chronic glomerulopathy; CI, confidence interval; ci, interstitial fibrosis; ct, tubular atrophy; cv, chronic vasculopathy; DSA, donor-specific antibody; GFR, glomerular filtration rate; HR, hazard ratio; SC-B-TCMR, subclinical borderline T cell-mediated rejection; SC-MVI, subclinical microvascular injury; SC-TCMR, subclinical T cell-mediated rejection; ti, total inflammation.