Abstract

BackgroundFibroblast growth factor 23 (FGF23) and endothelium-related biomarkers have been related to AKI in critically-ill patients. Also, FGF23 is associated with endothelial dysfunction. In this study, we investigated if elevated FGF23 association with severe AKI is mediated by several endothelial/glycocalyx-related biomarkers.MethodsProspective cohort study with critically-ill patients. Blood samples were collected within the first 24 h after ICU admission. Severe AKI (defined according to KDIGO stage 2/3) was the analyzed outcome.Results265 patients were enrolled and 82 (30.9%) developed severe AKI—defined according to KDIGO stage 2/3. Blood samples to biomarkers measurement were collected within the first 24 h after ICU admission. After adjustment for several variables, FGF23, vascular cell adhesion protein 1 (VCAM-1), angiopoietin 2 (AGPT2), syndecan-1 and intercellular adhesion molecule-1 (ICAM-1) were associated with severe AKI. The individual indirect effects of VCAM-1, AGPT2 and syndecan-1 explained 23%, 31%, and 32% of the total observed effect of FGF23 on severe AKI, respectively. ICAM-1 showed no statistically significant mediation. When all three endothelium-related biomarkers were included in a directed acyclic graph (DAG), the Bayesian network learning suggested the following causal association pathway FGF-23 → syndecan-1 → VCAM-1 → AGPT2 → severe AKI.ConclusionsThe association between FGF23 and AKI are mediated by endothelium-related biomarkers, mainly VCAM-1, AGPT2 and syndecan-1. Moreover, the statistical models show that syndecan-1, a biomarker of endothelial glycocalyx dysfunction, seems to be the initial mediator between FGF23 and severe AKI.

Highlights

  • Fibroblast growth factor 23 (FGF23) and endothelium-related biomarkers have been related to Acute kidney injury (AKI) in critically-ill patients

  • The statistical models show that syndecan-1, a biomarker of endothelial glycocalyx dysfunction, seems to be the initial mediator between FGF23 and severe AKI

  • In this cohort of criticallyill patients, we measured FGF23 and several endothelial-related biomarkers to test the hypothesis that the association of FGF23 and severe AKI could be mediated by endothelium/glycocalyx damage

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Summary

Introduction

Fibroblast growth factor 23 (FGF23) and endothelium-related biomarkers have been related to AKI in critically-ill patients. We investigated if elevated FGF23 association with severe AKI is mediated by several endothelial/glycocalyx-related biomarkers. Disordered mineral metabolism is a common complication of chronic kidney disease (CKD) [4], but only recently it has been studied in AKI [5,6,7,8,9]. Fibroblast growth factor (FGF) 23, a potent phosphaturic hormone released by osteocytes, play an important role in phosphate and vitamin D homeostasis and it is elevated in AKI [6,7,8]. FGF23 has emerged as a biomarker related to AKI and death in critically-ill patients [6, 7, 9] and following cardiac surgery [8]

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