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208 Prediction of Contrast Induced Nephropathy Using Novel Biomarkers Following Elective Contrast Coronary Angiography
  1. Michael Connolly1,
  2. Michelle Kinnin,
  3. David Mc Eneaney,
  4. Ian Menown,
  5. Neal Morgan,
  6. Mark Harbinson2
  1. 1Craigavon Area Hospital
  2. 2Queens University Belfast

Abstract

Introduction Chronic Kidney Disease (CKD) is a risk factor for contrast induced nephropathy (CIN), defined as an increase in serum creatinine of >25% from baseline or a delta rise of >26.5 µmol/L within 48 h. Early diagnosis of CIN requires validated novel biomarkers.

Methods A prospective observation study of 301 consecutive CKD patients undergoing elective invasive coronary angiography was performed. Low-osmolar contrast was standard. Demographics and Mehran risk score were recorded. Samples for plasma neutrophil gelatinase-associated lipocalin (NGAL), serum liver fatty acid-binding protein (L-FABP), serum kidney injury marker 1 (KIM-1), serum interleukin 18 (IL-18) and serum creatinine were taken at 0, 1, 2, 4, 6 and 48 h post contrast. Urinary NGAL and urinary cystatin C (CysC) were collected at 0, 6 and 48 h. Incidence of major adverse clinical events (MACE); acute myocardial infarction, heart failure hospitalisation, stroke and death were recorded at 1 year.

Results CIN occurred in 28 (9.3%) patients and were independently associated with older age, diabetes, higher Mehran score, larger contrast volume and anaemia (p < 0.05). Logistic regression analysis showed diabetes, CKD stage and GFR to be most predictive of CIN. The predictive power of plasma NGAL was greatest at 6 h with median levels of 1,337 ng/ml in CIN patients compared with 931 ng/ml in non-CIN patients (p = 0.002, AUC 0.71, sensitivity 75.0%, specificity 96.1%, OR 2.86), see figure 1 and table 1. L-FABP performed best at 4 h with median levels of 10.7 ng/ml in CIN patients compared with 6.2 ng/ml in non-CIN patients, p = 0.001, AUC 0.69, sensitivity 42.3%, specificity 90.2%, OR 6.75, Figure 1 and Table 1. Median urinary NGAL was higher only after 48 h, 487 ng/ml in CIN patients versus 155 ng/ml in non-CIN patients, p = 0.008, AUC 0.63. CysC, IL-18 and KIM-1 were not predictive at any time-point (p > 0.05). A Mehran score ≥10 performed prior to procedure achieved an AUC of 0.65, p = 0.006. MACE occurred in 7 (25.0%) CIN patients but only 17 (6.2%) non-CIN patients (p < 0.001). CIN cases also had considerably higher mortality (10.7% compared to 3.3%, p = 0.037). Exploratory analysis showed that the combination of Mehran score >10, 6 hr NGAL and 4 hr L-FABP improved specificity to 96.7%. Figure 2 highlights a proposed pathway of how biomarkers could be used to identify CIN early and facilitate timely therapeutic intervention to reduce morbidity and mortality.

Abstract 208 Figure 1

Median plasma NGAL (ng/ml) and serum L-FABP (ng/ml) in AKI and non-AKI

Abstract 208 Figure 2

Proposed patient pathways

Abstract 208 Table 1

Summary of NGAL (ng/ml) and L-FABP (ng/ml) in AKI and non-AKI patients


Conclusions/implications Mehran risk score, 6 h plasma NGAL and 4 h serum L-FABP performed best at early CIN prediction. CIN patients were four times more likely to develop MACE and had a trebling of mortality risk at 1 year. The implications of our results, translated to the design of safer elective coronary intervention services able to more efficiently manage the increasing volume of contrast studies, should be a key health priority for cardiac and renal services.

  • Contrast induced nephropathy
  • Biomarkers
  • Mehran score

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