JHLT open · 2026
Early biomarkers of acute kidney injury after lung transplantation.
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Scaravilli Vittorio, Uslenghi Alessandro, Turconi Gloria, Colombo Sebastiano Maria, Bosone Marco, Vago Valentina, Carrà Davide Pietro, Brivio Margherita, Morlacchi Letizia Corinna, Castellano Giuseppe, Zanella Alberto, Nosotti Mario, Rosso Lorenzo, Blasi Francesco, Grasselli Giacomo
Аннотация
BACKGROUND: Acute kidney injury (AKI) is common after lung transplantation (LUTX), with standard diagnostic criteria having limited early accuracy. We evaluated the AKI and postoperative outcomes risk-stratification performance of subclinical AKI and creatinine-independent kidney-injury phenotypes.
METHODS: In this prospective single-center cohort including bilateral LUTX recipients, we measured urinary Tissue Inhibitor of Metalloproteinases-2 and Insulin-Like Growth Factor-Binding Protein 7 (u[TIMP-2]*[IGFBP-7]) and plasma Heart-Type Fatty Acid-Binding Protein (H-FABP), midkine, Soluble Tumor Necrosis Factor Receptor 1 (sTNFR1), and sTNFR2 at 6 and 36 hours after reperfusion, using point-of-care devices. AKI was defined by KDIGO criteria. Subclinical AKI was defined as u[TIMP-2]*[IGFBP-7]>0.3 without AKI criteria. Creatinine-independent phenotypes were identified with outcome-agnostic Latent Profile Analysis (LPA).
RESULTS: Among 84 included patients, 30 (36%) developed AKI. u[TIMP-2]*[IGFBP-7] had modest AKI discrimination, with the best AUROC 0.63 (95%CI 0.58-0.70) at 36 hours. Twenty-five patients had subclinical AKI, which had outcomes similar to those of patients without AKI. At 36 hours, plasma H-FABP, sTNFR1, and sTNFR2 were higher in patients with AKI. LPA identified 3 classes: low-risk (30%), intermediate-risk (51%), and high-risk (19%), with increasing rates of AKI (16%, 42%, 72%; p = 0.006) and primary graft dysfunction grade 3 at 72 hours (4%, 13%, 35%; p = 0.045). Compared with the low-risk class, the high-risk class had fewer organ support-free, ICU-free, and hospital-free days and the lowest rejection-free survival.
CONCLUSIONS: After LUTX, u[TIMP-2]*[IGFBP-7] had limited risk-stratification performance, and subclinical AKI was not associated with a distinct clinical course. In contrast, plasma biomarker-derived risk phenotypes were associated with AKI severity and postoperative trajectory.
METHODS: In this prospective single-center cohort including bilateral LUTX recipients, we measured urinary Tissue Inhibitor of Metalloproteinases-2 and Insulin-Like Growth Factor-Binding Protein 7 (u[TIMP-2]*[IGFBP-7]) and plasma Heart-Type Fatty Acid-Binding Protein (H-FABP), midkine, Soluble Tumor Necrosis Factor Receptor 1 (sTNFR1), and sTNFR2 at 6 and 36 hours after reperfusion, using point-of-care devices. AKI was defined by KDIGO criteria. Subclinical AKI was defined as u[TIMP-2]*[IGFBP-7]>0.3 without AKI criteria. Creatinine-independent phenotypes were identified with outcome-agnostic Latent Profile Analysis (LPA).
RESULTS: Among 84 included patients, 30 (36%) developed AKI. u[TIMP-2]*[IGFBP-7] had modest AKI discrimination, with the best AUROC 0.63 (95%CI 0.58-0.70) at 36 hours. Twenty-five patients had subclinical AKI, which had outcomes similar to those of patients without AKI. At 36 hours, plasma H-FABP, sTNFR1, and sTNFR2 were higher in patients with AKI. LPA identified 3 classes: low-risk (30%), intermediate-risk (51%), and high-risk (19%), with increasing rates of AKI (16%, 42%, 72%; p = 0.006) and primary graft dysfunction grade 3 at 72 hours (4%, 13%, 35%; p = 0.045). Compared with the low-risk class, the high-risk class had fewer organ support-free, ICU-free, and hospital-free days and the lowest rejection-free survival.
CONCLUSIONS: After LUTX, u[TIMP-2]*[IGFBP-7] had limited risk-stratification performance, and subclinical AKI was not associated with a distinct clinical course. In contrast, plasma biomarker-derived risk phenotypes were associated with AKI severity and postoperative trajectory.