Abstract
BackgroundContrast-induced acute kidney injury (CI-AKI) particularly in high risk patients with chronic kidney disease (CKD), increases morbidity and mortality. Neutrophil gelatinase-associated lipocalin (NGAL) is a protein excreted by the kidney during AKI. There are no urine (u) NGAL data as an early CI-AKI marker in CKD patients undergoing coronary procedures.MethodsThis prospective study enrolled 130 patients with estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73 m2 undergoing elective coronary procedures. Serial urine samples, obtained at baseline and 3, 6, 12, 18, and 24 h post contrast administration were analyzed by NGAL ELISA kit. AKI was defined as an increase in serum creatinine (SCr) of ≥ 0.3 mg/dl or ≥ 1.5 times baseline SCr within 48 h per 2012 KDIGO guidelines. Receiver operator characteristic curve analyses identified optimal uNGAL and delta of uNGAL values for diagnosing CI-AKI.ResultsThe uNGAL was significantly and inverse correlated with eGFR (R = 0.25, P < 0.005). CI-AKI developed in 16/130 (12.31%) patients: 13 and 3 in CI-AKI stages I and II, respectively. uNGAL and delta of uNGAL were significantly higher in the CI-AKI group when compared with the No CI-AKI group (P < 0.05). The best uNGAL cut-off for optimal sensitivity 94%, specificity 78%, and area under the curve 0.84 for predicting CI-AKI was 117 ng/mL at 6 h, respectively. Corresponding values for predicting CI-AKI stage II were 100%, 87% and 0.9 when using an uNGAL of 264 ng/mL at 6 h.ConclusionsMonitoring of uNGAL levels not only provide the early detecting CI-AKI but also predict the severity of CI-AKI in CKD patients undergoing elective coronary procedures.
Highlights
Contrast-induced acute kidney injury (CI-AKI) in high risk patients with chronic kidney disease (CKD), increases morbidity and mortality
301 patients met the inclusion criteria based on a baseline estimated glomerular filtration rate (eGFR) < 60 mL/min. 171 patients were excluded from the study because 18 patients declined to participate, two patients suffered from congestive heart failure, three patients developed AKI and 148 patients were enrolled in other study
130 CKD patients were included in the present study: CKD stage III and CKD stage IV numbered 100 and 30 patients, respectively
Summary
Contrast-induced acute kidney injury (CI-AKI) in high risk patients with chronic kidney disease (CKD), increases morbidity and mortality. Contrast-induced acute kidney injury (CI-AKI) is one of the most common complications in patients who receive intravenous contrast media [1,2,3,4]. The incidence of CIAKI is low 1–2% in patients with normal renal function even with underlying diabetes mellitus [1] but increases up to 25% in patients with certified risk factors, for CI-AKI is defined as an acute deterioration in renal function after intravenous administration of contrast media by an absolute increase in serum creatinine (SCr) ≥ 0.5 mg/dL or ≥ 25% relative increase from baseline SCr within 48 hours after contrast media injection without evidence of other causes. Impairment of renal function in CI-AKI occurs within 3 days after intravenous administration of contrast media, while the peak of SCr is observed at 3– 5 days and returns to the baseline value within 1–3 weeks [9,10]. The earlier detection of CI-AKI with another biomarker/s could be diagnostically and therapeutically beneficial
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