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Kidney Week

Abstract: FR-OR10

Endotrophin, Released During Collagen Type VI Formation, Predicts Long-Term Mortality After AKI

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Sparding, Nadja, Nordic Bioscience, Herlev, Denmark
  • Rasmussen, Daniel Guldager Kring, Nordic Bioscience, Herlev, Herlev , Denmark
  • Genovese, Federica, Nordic Bioscience, Herlev, Herlev , Denmark
  • Karsdal, Morten Asser, Nordic Bioscience, Herlev, Herlev , Denmark
  • Packington, Rebecca A., Centre for Kidney Research and Innovation, University of Nottingham, Nottingham, United Kingdom
  • Selby, Nicholas M., Centre for Kidney Research and Innovation, University of Nottingham, Nottingham, United Kingdom

Group or Team Name

  • Fibrosis, Renal and Cardiovascular Research
Background

Acute kidney injury (AKI) is defined as a rapid decrease in kidney function which may be associated to structural damage. Early markers predicting AKI are emerging, but tools to monitor patients subsequent to AKI are still lacking. The novel biomarker PRO-C6 reflects formation of collagen type VI (COL6) and levels of endotrophin, a bioactive molecule derived from COL6. Here we evaluated the potential of PRO-C6 as a biomarker of mortality in AKI patients.

Methods

We measured PRO-C6 in plasma samples collected 1 year after the episode of AKI, using a novel ELISA in 801 patients from the AKI Risk in Derby (ARID) study, who were then followed prospectively until year three. 393 of the patients had been hospitalized for an episode of AKI, and 408 patients who did not sustain AKI were included as controls (non-AKI). The groups were matched for age, baseline renal function and diabetes.

Results

PRO-C6 levels were significantly higher in the AKI compared to the non-AKI group (median (m): 10.85 vs 9.23 ng/mL, P<0.0001). By year 3, a total of 70 patients died; 43 in the AKI group and 27 in the control group. In the AKI group, patients who died had significantly higher PRO-C6 levels than the patients who did not die (m: 12.66 vs 10.68 ng/mL, P=0.004), whereas there was no difference between patients who died and did not die in the non-AKI group (m: 9.97 vs 9.21 ng/mL, P=0.23). In a multivariate Cox regression analysis with backwards elimination including age, gender, baseline CKD and diabetes status, albuminuria, serum creatinine, eGFR and PRO-C6, only age (P=0.04) and albuminuria (P=0.007) remained in the final model for the non-AKI group. In the AKI group, PRO-C6 had a stronger association with mortality than eGFR, as only age (P=0.005), albuminuria (P=0.04) and PRO-C6 (P=0.004) remained in the final model. When stratified into tertiles, patients with higher levels of PRO-C6 at year 1 were significantly more likely to die (P=0.009).

Conclusion

In this study, we compared levels of PRO-C6 in patients with and without AKI, and show that PRO-C6 levels measured in plasma can predict mortality in patients with AKI. Our findings may indicate that PRO-C6 identifies patients with active fibrogenesis after AKI, suggesting that long-term renal injury after AKI is important for patient outcome.