PGD Is Associated With Persistent Differential Gene Expression After Lung Transplantation

s S171 585 LRTx recipients. Uniand multivariate Cox regression assessed the effect of recipient, operative, donor, and hospital characteristics on survival. Propensity score matching accounted for baseline differences, and Kaplan-Meier analysis evaluated post-transplant survival in un-matched and matched groups. Results: Before matching, LRTx patients had a greater frequency of ECMO support, mechanical ventilation, and renal insufficiency, and were less likely to receive double LTx (table 1). Given these worse comorbidities, one would expect the inferior survival found in LRTx recipients (figure 1a). Propensitymatching was able to balance covariates between LTx and LRTx groups (table 1). Even after accounting for preoperative characteristics, there remained a significant association between LRTx and death in our matched survival analysis (figure 1b). Multivariable Cox regression confirmed this finding, with LRTx having a hazard ratio of 1.26 for death (95% confidence interval 1.09-1.45). Other risk factors for death are shown in table 1. Conclusion: Even after accounting for recipient, operative, donor, and hospital characteristics, LRTx recipients had worse survival compared with LTx recipients. The independent association between LRTx and death warrants consideration for including LRTx status into the LAS. Demographics, comorbidities, operative, and hospital characteristics before and after matching Firsttime, all (n= 11,294) Redo, all (n= 585) Standardized Difference First-time, matched (n= 524) Redo, matched (n= 524) Standardized Difference Hazard Ratio for death Age, y 54.6±13.0 47.4±15.6 -0.502 49.0 48.2 -0.055 1.011 (1.0081.015) Male gender 6660 (59.0) 334 (57.1) -0.038 309 (59.0) 306 (58.4) -0.012 1.09 (1.011.17) AfricanAmerican race 958 (8.5) 34 (5.8) -0.104 29 (5.5) 32 (6.1) 0.024 0.86 (0.750.98) Private insurance 6308 (56.0) 305 (52.6) -0.069 267 (51.3) 271 (52.1) 0.017 0.89 (0.830.95) BMI, kg/m2 25.2±4.7 22.8±4.8 -0.501 23.1±2.7 23.0±4.8 -0.005 1.001 (0.9931.010) Previous lung transplant 0 (0.0) 585 (100) 0 (0.0) 524 (100) 1.26 (1.091.45) Diagnosis of idiopathic pulmonary fibrosis 4134 (36.6) 156 (26.7) -0.215 159 (30.3) 148 (28.2) -0.046 1.00 (used as baseline diagnosis) Diagnosis of chronic obstructive pulmonary disease 3174 (28.1) 120 (20.5) -0.178 114 (21.8) 112 (21.4) -0.009 0.91 (0.840.99) NYHA IV symptoms 1401 (12.4) 168 (27.7) 0.412 129 (24.6) 142 (27.1) 0.057 1.35 (1.241.47) 6-minute walk, ft 777±438 657±504 -0.254 688±463 656±496 -0.065 0.99975 (0.999670.99982) Ventilator 546 (4.8) 146 (25.0) 0.589 108 (20.6) 121 (23.1) 0.060 1.21 (1.041.40) ECMO 145 (1.3) 29 (5.0) 0.212 18 (3.4) 26 (5.0) 0.076 1.72 (1.312.26) Creatinine clearance, ml/min 102±32 81±34 -0.659 82±26 83±34 0.032 1.16 (1.031.31) High performing institution 4362 (38.6) 183 (31.3) -0.154 167 (31.9) 167 (31.9) 0.79 (0.740.84) Moderateor high-volume institution 8126 (72.0) 447 (76.4) 0.102 383 (73.1) 402 (76.7) 0.084 0.76 (0.710.82) Double lung transplant 7440 (65.9) 305 (52.1) -0.282 278 (53.1) 279 (53.2) 0.004 0.82 (0.760.88) Race match, n (%) 7744 (68.6) 383 (65.5) -0.066 290 (55.3) 277 (52.9) -0.050 0.88 (0.820.94) Complete HLA mismatch (all 6 alleles) 2208 (22.3) 105 (20.4) -0.047 110 (24.3) 89 (19.3) -0.123 1.11 (1.031.20) Panelreactive antibody ≥ 20% 985 (9.4) 75 (14.1) 0.145 53 (11.0) 62 (13.0) 0.060 1.18 (1.051.33) fold, FDR< 0.05) at least 7 days after transplant.11 gene products were differentially expressed in PGD vs. non-PGD subjects. Three gene products, PTX3, IL18R1, and NLRC4, all associated with innate immune and inflammatory responses, were increased throughout the first year after transplant (Table 1). Conclusion: The differences in gene expression associated with PGD persist for several weeks after transplant. Persistent alteration in gene expression amongst genes responsible for innate immune regulation and T-cell function may provide a pathologic link between PGD and long-term allograft dysfunction.