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. 2020 Nov 17;10(1):20005.
doi: 10.1038/s41598-020-76929-y.

Acute kidney injury risk in orthopaedic trauma patients pre and post surgery using a biomarker algorithm and clinical risk score

Mary Jo Kurth  1 , William T McBride  2 , Gavin McLean  3 , Joanne Watt  1 , Anna Domanska  1 , John V Lamont  1 , Daniel Maguire  1 , Peter Fitzgerald  1 , Mark W Ruddock  4
Affiliations

Acute kidney injury risk in orthopaedic trauma patients pre and post surgery using a biomarker algorithm and clinical risk score

Mary Jo Kurth et al. Sci Rep. .

Abstract

Acute kidney injury (AKI) after major trauma is associated with increased mortality. The aim of this study was to assess if measurement of blood biomarkers in combination with clinical characteristics could be used to develop a tool to assist clinicians in identifying which orthopaedic trauma patients are at risk of AKI. This is a prospective study of 237 orthopaedic trauma patients who were consecutively scheduled for open reduction and internal fixation of their fracture between May 2012 and August 2013. Clinical characteristics were recorded, and 28 biomarkers were analysed in patient blood samples. Post operatively a combination of H-FABP, sTNFR1 and MK had the highest predictive ability to identify patients at risk of developing AKI (AUROC 0.885). Three clinical characteristics; age, dementia and hypertension were identified in the orthopaedic trauma patients as potential risks for the development of AKI. Combining biomarker data with clinical characteristics allowed us to develop a proactive AKI clinical tool, which grouped patients into four risk categories that were associated with a clinical management regime that impacted patient care, management, length of hospital stay, and efficient use of hospital resources.

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Conflict of interest statement

YES, M.J.K., A.D., D.M., J.W., J.V.L., and M.W.R. are employees of Randox Laboratories Ltd but hold no shares in the Company. P.F. is the Managing Director and owner of Randox, a privately-owned Company. G.M. was funded by Randox Laboratories Ltd, 55 Diamond Road, Crumlin BT29 4QY for 2 years to complete his MD. W.M. has no competing interests. A patent has been submitted by Randox to protect the biomarkers identified from this work.

Figures

Figure 1
Figure 1
Trial flow diagram. AKI acute kidney injury.
Figure 2
Figure 2
(A) Pre surgery serum biomarker predicted probabilities for AKI development post operatively. H-FABP, MK, sTNFR1 and sTNFR2 predicted probabilities for preoperative serum levels. Wilcoxon rank sum statistical significance is indicated by *p ≤ 0.05, **p ≤ 0.01, ****p ≤ 0.0001. AKI acute kidney injury, H-FABP heart-type fatty acid-binding protein, MK midkine, sTNFR soluble tumour necrosis factor receptor. (B) Receiver operator characteristics for pre surgery serum biomarkers. H-FABP (AUROC 0.712), MK (AUROC 0.615), sTNFR1 (AUROC 0.729) and sTNFR2 (AUROC 0.634). AUROC area under the receiver operator characteristic, H-FABP heart-type fatty acid-binding protein, MK midkine, sTNFR soluble tumour necrosis factor receptor.
Figure 3
Figure 3
(A) Post operative serum biomarker model predicted probabilities for non AKI and AKI patients. Predicted probabilities for post surgery serum levels for H-FABP, MK and sTNFR1 individually and combined. Wilcoxon rank sum statistical significance is indicated by: **p <  = 0.01, ****p <  = 0.0001. AKI acute kidney injury, H-FABP heart-type fatty acid-binding protein, MK midkine, sTNFR soluble tumour necrosis factor receptor. (B) Receiver operator characteristics for post surgery serum biomarkers and model. H-FABP (AUROC 0.829), MK (AUROC 0.678), sTNFR1 (AUROC 0.795) and model H-FABP + MK + sTNFR1 (AUROC 0.885). AUROC area under the receiver operator characteristic, H-FABP heart-type fatty acid-binding protein, MK midkine, sTNFR soluble tumour necrosis factor receptor.
Figure 4
Figure 4
Pathogenesis of AKI. Three important pathways in the pathogenesis of AKI are represented by biomarkers in the model: (1) hypoperfusion (H-FABP), (2) proinflammation (sTNFR1 as a surrogate for the transient TNFα response) and (3) ischaemia reperfusion injury (MK). Adapted from McBride et al.. AKI acute kidney injury, BP blood pressure, H-FABP heart-type fatty acid-binding protein, MK midkine, sTNFR soluble tumour necrosis factor receptor, TNFα tumour necrosis factor alpha.
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