title: Novel Biomarkers of Acute Kidney Injury After Contrast Coronary Angiography.
abstract: Acute kidney injury (AKI), defined as a rise in serum creatinine of greater than 25% from baseline measured at 48 hours after renal insult, may follow iodinated contrast coronary angiography. Termed contrast-induced nephropathy, it can result in considerable morbidity and mortality. Measurement of serum creatinine as a functional biomarker of glomerular filtration rate is widely used for detection of AKI, but it lacks sensitivity for the early diagnosis of AKI (typically rising 24 hours after functional loss) and, as a solely functional marker of glomerular filtration rate, is unable to differentiate among the various causes of AKI. These intrinsic limitations to creatinine measurement and the recognition that improved clinical outcomes are linked to a more timely diagnosis of AKI, has led investigators to search for novel biomarkers of "early" kidney injury. Several studies have investigated the utility of renal injury biomarkers in a variety of clinical settings including angiography/percutaneous coronary intervention, coronary artery bypass graft surgery, sepsis in intensive care patients, and pediatric cardiac surgery. In this article, we discuss the use of iodinated contrast for coronary procedures and the risk factors for contrast-induced nephropathy, followed by a review the potential diagnostic utility of several novel biomarkers of early AKI in the clinical settings of coronary angiography/percutaneous coronary intervention. In particular, we discuss neutrophil gelatinase associated lipocalin in depth. If validated, such biomarkers would facilitate earlier AKI diagnosis and improve clinical outcomes.
authors.affiliation: From the *Cardiovascular Research Unit, Craigavon Cardiac Centre, Southern Trust, Northern Ireland, United Kingdom; †Department of Nephrology, Daisy Hill Hospital, Southern Trust, Northern Ireland, United Kingdom; and ‡Centre for Experimental Medicine, Queens University Belfast, Northern Ireland, United Kingdom.
authors.forename: M
authors.initials: M
authors.lastname: Connolly
authors.forename: D
authors.initials: D
authors.lastname: McEneaney
authors.forename: Ian
authors.initials: I
authors.lastname: Menown
authors.forename: N
authors.initials: N
authors.lastname: Morgan
authors.forename: M
authors.initials: M
authors.lastname: Harbinson
mesh_terms: D000118:Acetylglucosaminidase / Q000097:blood; D058186:Acute Kidney Injury / Q000097:blood / Q000139:chemically induced* / Q000175:diagnosis; D000209:Acute-Phase Proteins; D015415:Biomarkers; D003287:Contrast Media / Q000009:adverse effects*; D017023:Coronary Angiography; D003404:Creatinine / Q000097:blood; D055316:Cystatin C / Q000097:blood; D050556:Fatty Acid-Binding Proteins / Q000097:blood; D000072596:Hepatitis A Virus Cellular Receptor 1; D006801:Humans; D020382:Interleukin-18 / Q000097:blood; D017613:Iodine Compounds / Q000009:adverse effects*; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood; D008562:Membrane Glycoproteins / Q000097:blood*; D062645:Percutaneous Coronary Intervention; D011518:Proto-Oncogene Proteins / Q000097:blood; D011991:Receptors, Virus / Q000097:blood*; D012680:Sensitivity and Specificity
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; C525030:CST3 protein, human; D003287:Contrast Media; D055316:Cystatin C; C493319:FABP1 protein, human; D050556:Fatty Acid-Binding Proteins; C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D020382:Interleukin-18; D017613:Iodine Compounds; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; D011991:Receptors, Virus; D003404:Creatinine; D000118:Acetylglucosaminidase