| Autor: |
Cerier, Emily, Kurihara, Chitaru, Kaiho, Taisuke, Toyoda, Takahide, Manerikar, Adwaiy, Kandula, Viswajit, Thomae, Benjamin, Yagi, Yuriko, Yeldandi, Anjana, Kim, Samuel, Avella-Patino, Diego, Pandolfino, John, Perlman, Harris, Singer, Benjamin, Scott Budinger, G.R., Lung, Kalvin, Alexiev, Borislav, Bharat, Ankit |
| Zdroj: |
American journal of transplantation; 20230101, Issue: Preprints |
| Abstrakt: |
Growing evidence implicates complement in the pathogenesis of primary graft dysfunction (PGD). We hypothesized that early complement activation postreperfusion could predispose to severe PGD grade 3 (PGD-3) at 72 hours, which is associated with worst posttransplant outcomes. Consecutive lung transplant patients (n = 253) from January 2018 through June 2023 underwent timed open allograft biopsies at the end of cold ischemia (internal control) and 30 minutes postreperfusion. PGD-3 at 72 hours occurred in 14% (35/253) of patients; 17% (44/253) revealed positive C4d staining on postreperfusion allograft biopsy, and no biopsy-related complications were encountered. Significantly more patients with PGD-3 at 72 hours had positive C4d staining at 30 minutes postreperfusion compared with those without (51% vs 12%, P< .001). Conversely, patients with positive C4d staining were significantly more likely to develop PGD-3 at 72 hours (41% vs 8%, P< .001) and experienced worse long-term outcomes. In multivariate logistic regression, positive C4d staining remained highly predictive of PGD-3 (odds ratio 7.92, 95% confidence interval 2.97-21.1, P< .001). Hence, early complement deposition in allografts is highly predictive of PGD-3 at 72 hours. Our data support future studies to evaluate the role of complement inhibition in patients with early postreperfusion complement activation to mitigate PGD and improve transplant outcomes. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
