SLPI and CXCL10 in non-obese patients, and Serpin E1 in obese patients as AKI biomarkers after cardiac surgery

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Abstract

Introduction

Acute kidney injury (AKI) is a common complication after cardiac surgery, affecting 18% of patients and significantly increasing the risk of mortality. AKI triggers the release of proinflammatory molecules during cardiopulmonary bypass. Obesity, characterised by chronic low-grade inflammation, is an established risk factor for AKI; however, the association between obesity, inflammation and AKI is complex and poorly understood. We investigated the utility of inflammatory molecules in the diagnosis of AKI post-cardiac surgery in obese and non-obese patients.

Methods

A panel of 14 circulating plasma molecules (CXCL1, 10 and 13, CCL22, IL-5, 6, 8, 10 and 16, SLPI, TIM1, Properdin, Serpins E1 and A3) was measured using MAGPIX analyser or ELISA kits in samples collected from 95 MaRACAS patients ( NCT02315183 ) before and 6-96 hours after surgery.

Results

There was no significant difference in the incidence of AKI between obese (46%) and non-obese (58%) patients. In non-obese patients with AKI, levels of CXCL10, CXCL13, SLPI, and IL-16 were all significantly higher immediately after surgery. SLPI showed the strongest and most consistent association with AKI, with significant predictive value at 6-12, 24 and 72 hours (ROC AUCs 77.7%, 86.3%, and 89.8%). CXCL10 was also associated with AKI at 6-12 hours and 48 hours (ROC AUCs of 84.5% and 72.9%). In obese patients with AKI, Serpin E1 was significantly lower before surgery, but increased at 6-12 hours, showing a significant association with AKI (ROC AUCs 66.7% pre-op and 71.2% at 6–12 hours). Properdin was also significantly higher in obese patients with AKI at 72 hours (ROC AUC of 85%). Other measured biomarkers did not differ between AKI and non-AKI groups in either obese or non-obese patients.

Conclusions

Distinct dynamic changes of SLPI and CXCL10 in non-obese and Serpin E1 and Properdin in obese patients have diagnostic potential as biomarkers of AKI post-cardiac surgery. These proinflammatory molecules should be further validated in larger cohorts.

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