Prediction of contrast induced acute kidney injury using novel biomarkers following contrast coronary angiography

M. Connolly*, M. Kinnin, D. McEneaney, I. Menown, M. Kurth, J. Lamont, N. Morgan, M. Harbinson

*Corresponding author for this work

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Abstract

Background/Introduction: Chronic kidney disease (CKD) is a risk factor for contrast induced acute kidney injury (CI-AKI). Contrast angiography in CKD patients is a common procedure. Creatinine is a delayed marker of CI-AKI and delays diagnosis which results in significant morbidity and mortality. Aim: Early diagnosis of CI-AKI requires validated novel biomarkers. Design: A prospective observation study of 301 consecutive CKD patients undergoing coronary angiography was performed. Methods: Samples for plasma neutrophil gelatinase-associated lipocalin (NGAL), serum liver fatty acid-binding protein (LFABP), serum kidney injury marker 1, serum interleukin 18 and serum creatinine were taken at 0, 1, 2, 4, 6 and 48h postcontrast. Urinary NGAL and urinary cystatin C were collected at 0, 6 and 48 h. Incidence of major adverse clinical events (MACE) was recorded at 1 year. CI-AKI was defined as an absolute delta rise in creatinine of ≥ 26.5 μmol/l or a 50% relative rise from baseline at 48h following contrast. Results: CI-AKI occurred in 28 (9.3%) patients. Plasma NGAL was most predictive of CI-AKI at 6 h. L-FABP performed best at 4h. A combination of Mehran score > 10, 4h L-FABP and 6h NGAL improved specificity to 96.7%. MACE was statistically higher at 1 year in CI-AKI patients (25.0 vs. 6.2% in non-CI-AKI patients). Discussion/Conclusion: Mehran risk score, 4h serum L-FAPB and 6 h plasma NGAL performed best at early CI-AKI prediction. CI-AKI patients were four times more likely to develop MACE and had a trebling of mortality risk at 1 year.Background/Introduction: Chronic kidney disease (CKD) is a risk factor for contrast induced acute kidney injury (CI-AKI). Contrast angiography in CKD patients is a common procedure. Creatinine is a delayed marker of CI-AKI and delays diagnosis which results in significant morbidity and mortality. Aim: Early diagnosis of CI-AKI requires validated novel biomarkers. Design: A prospective observation study of 301 consecutive CKD patients undergoing coronary angiography was performed. Methods: Samples for plasma neutrophil gelatinase-associated lipocalin (NGAL), serum liver fatty acid-binding protein (LFABP), serum kidney injury marker 1, serum interleukin 18 and serum creatinine were taken at 0, 1, 2, 4, 6 and 48h postcontrast. Urinary NGAL and urinary cystatin C were collected at 0, 6 and 48 h. Incidence of major adverse clinical events (MACE) was recorded at 1 year. CI-AKI was defined as an absolute delta rise in creatinine of≥26.5 mmol/l or a 50% relative rise from baseline at 48h following contrast. Results: CI-AKI occurred in 28 (9.3%) patients. Plasma NGAL was most predictive of CI-AKI at 6 h. L-FABP performed best at 4h. A combination of Mehran score > 10, 4h L-FABP and 6h NGAL improved specificity to 96.7%. MACE was statistically higher at 1 year in CI-AKI patients (25.0 vs. 6.2% in non-CI-AKI patients). Discussion/Conclusion: Mehran risk score, 4h serum L-FAPB and 6 h plasma NGAL performed best at early CI-AKI prediction. CI-AKI patients were four times more likely to develop MACE and had a trebling of mortality risk at 1 year.

Original languageEnglish
Pages (from-to)103-110
Number of pages8
JournalQJM
Volume111
Issue number2
DOIs
Publication statusPublished - 23 Oct 2017

ASJC Scopus subject areas

  • Medicine(all)

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    Connolly, M., Kinnin, M., McEneaney, D., Menown, I., Kurth, M., Lamont, J., Morgan, N., & Harbinson, M. (2017). Prediction of contrast induced acute kidney injury using novel biomarkers following contrast coronary angiography. QJM, 111(2), 103-110. https://doi.org/10.1093/qjmed/hcx201