Neutrophil gelatinase associated lipocalin as a biomarker for acute kidney injury in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass

Abstract

Background: Acute kidney injury (AKI) is a significant cause of morbidity and mortality following cardiac surgery throughout the world. The paucity of early biomarkers has hampered early therapeutic intervention. Our aim was to evaluate plasma neutrophil gelatinase associated lipocalin (NGAL) levels as a predictor of renal injury in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB) along with markers of oxidative stress.

Methods: About 30 patients undergoing CABG with CPB were prospectively studied. Blood was collected before bypass, at 4, 12, and 24 hr after CPB initiation, for the analysis of NGAL and oxidative stress markers.

Results: Eight of 30 patients (26.6%) developed AKI, while 22 (73.4%) did not, as measured by serum creatinine, after 48-72 hr of surgery. However, plasma NGAL levels at 4 hr were high in patients who developed AKI compared with those who did not (352.97 +/- 49.32 vs. 199.83 +/- 23.28 ng/mL, p = 0.000). There was a significant difference in aortic cross-clamp time (p = 0.000), duration of CPB (p = 0.000), and ventilation duration (p < 0.05) between the two groups. The level of malondialdehyde (MDA), a marker of oxidative stress, was higher only at 4 hr in the AKI group. No significant differences were observed in the level of antioxidants between the two groups. A significant correlation was found between plasma NGAL at 4 hr and the change in serum creatinine (r = 0.863, p = 0.006) as well as ventilation duration (r = 0.830, p = 0.011). The sensitivity and specificity of plasma NGAL at 4 hr after CPB was optimal at the 229 ng/mL cut-off with an area under the curve of 0.98 for prediction of AKI.

Conclusion: Measurement of plasma NGAL in patients in the first few hours after CPB is predictive of AKI. Oxidative stress as measured by the level of MDA and antioxidants has no substantial role in the progression of AKI during CABG with CPB.