ArticleJHLT open2026
Early biomarkers of acute kidney injury after lung transplantation.
Article in JHLT open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
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Abstract
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%; 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.
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