17-P

Abstract

Angiotensin II type 1 receptor (AT1R) is found in lung alveolar epithelium, the stroma surrounding epithelial layer of small airways, fibroblasts, vessel smooth muscle and alveolar macrophages. While the impact of HLA antibody in lung rejection is increasingly recognized, this association has not been studied for non-HLA antibodies such as anti-AT1R antibodies. We studied 112 patients who underwent lung transplantation in our center since the inception of the lung allocation score (LAS) in May 2005. Pre-transplant sera were screened for HLA and AT1R antibodies. 89 patients had clinical data available for analysis. AT1R antibody was tested on an ELISA platform while HLA antibody was defined using solid phase luminometric assays. AT1R levels were examined as continuous values. Test results were interpreted using a dichotomized cut-point of 17 U/ml as recommended by the manufacturer. AT1R antibodies were positive in 31(35%) and negative in 58(65%) patients. Gender was not associated with AT1R sensitization (p = 0.2). Donor HLA specific antibodies were found in 10(11%) patients who were excluded from lung function and survival analysis. AT1R sensitization was not a significant predictor for lung function at 48 hours (p = 0.07) or at 6 month (p = 0.9). Further, presence of AT1R antibodies did not correlate with one year patient survival by Kaplan-Meier method (p = 0.8). AT1R sensitization was not a risk factor for rejection within 1 year (p = 0.5) or >1 year (p = 0.7) post-transplant. Post-transplant acute kidney injury was not associated with presence of AT1R antibodies. Post-operative care was also similar between the two groups (median length of stay in ICU, p = 0.9; median total hospital length of stay, p = 0.6). Our data show that AT1R sensitization does not correlate with early clinical outcomes in lung transplantation.