The plasma level and biomarker value of neutrophil gelatinase-associated lipocalin in critically ill patients with acute kidney injury are not affected by continuous venovenous hemofiltration and anticoagulation applied

• Published in: Critical care (London, England) Vol. 18; no. 2; p. R78
• Main Authors: Schilder, Louise, Nurmohamed, S Azam, ter Wee, Pieter M, Paauw, Nanne J, Girbes, Armand R J, Beishuizen, Albertus, Beelen, Robert H J, Groeneveld, A B Johan
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 22.04.2014; BioMed Central
• Subjects: Acute Kidney Injury - blood; Acute Kidney Injury - mortality; Acute Kidney Injury - therapy; Acute-Phase Proteins; Adult; Aged; Aged, 80 and over; Anticoagulants - therapeutic use; Biomarkers - blood; Critical Illness - therapy; Female; Hemofiltration - methods; Humans; Lipocalin-2; Lipocalins - blood; Male; Middle Aged; Prospective Studies; Proto-Oncogene Proteins - blood; Survival Rate - trends; Treatment Outcome; Young Adult
• ISSN: 1364-8535; 1466-609X; 1364-8535
• DOI: 10.1186/cc13838

Neutrophil gelatinase-associated lipocalin (NGAL) is a biomarker of acute kidney injury (AKI), and levels reflect severity of disease in critically ill patients. However, continuous venovenous hemofiltration (CVVH) may affect plasma levels by clearance or release of NGAL by activated neutrophils in the filter, dependent on the anticoagulation regimen applied. We therefore studied handling of NGAL by CVVH in patients with AKI. Immediately before initiation of CVVH, prefilter blood was drawn. After 10, 60, 180, and 720 minutes of CVVH, samples were collected from pre- and postfilter (in- and outlet) blood and ultrafiltrate. CVVH with the following anticoagulation regimens was studied: no anticoagulation in case of a high bleeding tendency (n = 13), unfractionated heparin (n = 8), or trisodium citrate (n = 21). NGAL levels were determined with enzyme-linked immunosorbent assay (ELISA). Concentrations of NGAL at inlet and outlet were similar, and concentrations did not change over time in any of the anticoagulation groups; thus no net removal or production of NGAL occurred. Concentrations of NGAL at inlet correlated with disease severity at initiation of CVVH and at the end of a CVVH run. Concentrations of NGAL in the ultrafiltrate were lower with citrate-based CVVH (P = 0.03) and decreased over time, irrespective of anticoagulation administered (P < 0.001). The sieving coefficient and clearance of NGAL were low and decreased over time (P < 0.001). The plasma level and biomarker value of NGAL in critically ill patients with AKI are not affected by CVVH, because clearance by the filter was low. Furthermore, no evidence exists for intrafilter release of NGAL by neutrophils, irrespective of the anticoagulation method applied.