Open AccessBiomarkers in the prediction of contrast media induced nephropathy – the BITCOIN study
Author(s) -
Felix S. Seibert,
Anja Heringhaus,
Nikolaos Pagonas,
Henrik Rudolf,
Benjamin Rohn,
Frederic Bauer,
Nina Timmesfeld,
HansJoachim Trappe,
Nina Babel,
Timm H. Westhoff
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0234921
Subject(s) - medicine , creatinine , renal function , acute kidney injury , kidney disease , urology , gastroenterology , proteinuria , area under the curve , contrast induced nephropathy , urinary system , biomarker , receiver operating characteristic , nephropathy , cystatin c , prospective cohort study , kidney , endocrinology , percutaneous coronary intervention , myocardial infarction , biochemistry , chemistry , diabetes mellitus
Background Subjects with chronic kidney disease are at increased risk for contrast-induced acute kidney injury (CI-AKI). Risk stratification is traditionally based on glomerular filtration rate (GFR) and proteinuria. The present trial examines, whether tubular and inflammatory biomarkers are able to identify subjects at increased risk as well. Methods We performed a prospective study in 490 patients undergoing coronary angiography. An increase of serum creatinine concentration ≥ 0.3 mg/dl from baseline to day 2–3 was defined as primary endpoint (CI-AKI). Urinary neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and calprotectin were assessed < 24h before coronary angiography. Prognostic accuracy was assessed by receiver operating characteristics (ROC) calculations. Results 30 (6.1%) patients suffered from CI-AKI (27 AKIN stage I, 3 AKIN stage II, 0 AKIN stage III). Those subjects who developed CI-AKI had 3.1 fold higher baseline urinary NGAL/creatinine ratios than those without CI-AKI (60.8 [IQR 18.7–93.1] μg/mg vs. 19.9 [IQR 12.3–38.9] μg/mg, p = 0.001). In those subjects without clinically overt CKD (eGFR > 60 ml/min, urinary albumin creatinine ratio <30 mg/g), the NGAL/creatinine ratio was 2.6 higher in CI-AKI vs. no CI-AKI (47.8 [IQR 11.8–75.3] vs. 18.6 [IQR 11.7–36.3] μg/mg). No significant differences were obtained for KIM-1 and calprotectin (p>0.05 each). ROC analyses revealed an area under the curve (AUC) of 0.68 (95% CI 0.60–0.81) for NGAL/creatinine. An NGAL/creatinine ratio < 56.4 μg/mg has a negative predictive value of 96.5%. Conclusions The present study is the largest investigation on the use of urinary biomarkers for CI-AKI risk stratification so far. It shows that NGAL provides prognostic information beyond the glomerular biomarkers eGFR and proteinuria.