Acute kidney injury (AKI) is a common complication following cardiac surgery with cardiopulmonary bypass (CPB). This study investigated whether cell-free hemoglobin (CFHb) levels after CPB are associated with endothelial damage and postoperative AKI in patients with preexisting renal dysfunction.

A substudy of a randomized controlled trial.

Secondary referral and tertiary hospital.

Adult patients undergoing cardiac surgery with CPB and an estimated glomerular filtration rate (eGFR) <50 mL/min/1.73 m² or diabetes mellitus with an eGFR of <60 mL/min/1.73 m².

Clinical data and plasma samples were collected after induction of anesthesia, within 1 hour at the intensive care unit, and 24 and 48 hours postoperatively.

Of the 89 patients included, 21% developed AKI. CFHb peaked at 1 hour postoperatively (22.5 v 5.4 mg/dL, p < 0.001), and lactate dehydrogenase rose until 48 hours postoperatively (119 v 339 U/L, p < 0.001). Tumor necrosis factor α and intercellular adhesion molecule 1 increased following surgery (7.06 v 9.21 ng/mL, p = 0.020; 247 v 388 ng/mL, p < 0.001). Angiopoietin-2 rose until 48 hours postoperatively and was higher in patients with AKI at 24 hours (4,162 v 3,374 pg/mL, p = 0.027). Similarly, neutrophil gelatinase-associated lipocalin increased in patients with AKI (43.1 v 88.0 ng/mL, p < 0.001). CFHb at 1 hour postoperatively was not associated with angiopoietin-2 at 24 or 48 hours. Adding CFHb to a prediction model of AKI did not improve model fit (p = 0.28) or discrimination (p = 0.32).

This study demonstrates that CPB induces hemolysis and endothelial activation and damage in patients with preexisting renal dysfunction. Although CFHb concentrations were higher in those developing AKI, CFHb did not predict AKI or correlate with markers of endothelial damage.