Urine IL-18, NGAL, IL-8 and serum IL-8 are biomarkers of acute kidney injury following liver transplantation

Abstract

BackgroundAKI is common following liver transplantation and is associated with significant morbidity and mortality. Biomarkers of AKI have not been well established in this setting but are needed to help guide patient care and facilitate development of novel therapeutics.MethodsSerum creatinine, cystatin C, IL-6, and IL-8 and urine IL-18, NGAL, IL-6, and IL-8 were measured before and within 24 hours after liver transplantation in 40 patients. AKI was defined as a ≥50% sustained increase in creatinine above pre-operative values occurring within 24 hours of transplantation and persisting for at least 24 hours.ResultsSeven patients met criteria for AKI (17.5%), with mean creatinines of 0.81 mg/dL pre-operatively and 1.75 mg/dL post-operatively. While pre-operative biomarker levels in patients with AKI were similar to those in patients without AKI, differences were seen between the groups with regard to median post-operative serum IL-8 (pg/mL) (242.48 vs. 82.37, p = 0.0463) and urine NGAL (ng/mL) (386.86 vs. 24.31, p = 0.0039), IL-6 (pg/mL) (52 vs. 7.29, p=0.0532), IL-8 (pg/mL) (14.3 vs. 0, p = 0.0224), and IL-18 (pg/mL) (883.09 vs. 0, p = 0.0449). The areas under receiver operating characteristic (ROC) curves were 0.749 for urine IL-18, 0.833 for urine NGAL, 0.745 for urine IL-6, 0.682 for serum IL-6, 0.773 for urine IL-8, and 0.742 for serum IL-8. Post-operative cystatin C was not significantly different between AKI and no AKI groups.ConclusionSerum IL-8 and urine IL-18, NGAL, IL-6, and IL-8 are elevated in AKI within the first 24 hours following liver transplantation.

The ameliorative potential of Hyphaene thebaica on streptozotocin-induced diabetic nephropathy

“…Neutrophil gelatinase--associated lipocalin (NGAL) is a biomarker expressed in numerous human tissues, including the kidney, and is of significant expression within injured epithelia [39]. NGAL genes have been found to be strongly expressed following renal ischaemic or nephrotoxic injuries in animal models [36].…”

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“…Early detection biomarkers for CI-AKI include cystatin C, a renal function marker with a shorter half-life than creatinine [12], and others related to the possible pathogenic mechanisms of CI-AKI such as renal tubular damage, oxidative stress, inflammation and apoptosis [13,14,15,16,17,18]. …”

Evaluation of serum cysteine-rich protein 61 and cystatin C levels for assessment of acute kidney injury after cardiac surgery

“…24 Conversely, Sirota et al showed that serum creatinine level was significantly decreased pre-operatively in AKI group in comparison to non-AKI group; and was overexpressed post-operatively in AKI group than non-AKI. 25 In contrast to adult population, a study which was carried out on pediatric cardiac patients by Peco-Antić et al stated that no significant change was observed in serum creatinine baseline between AKI and non-AKI groups. 26 Rosner and Moran et al explained the increase in CysC levels in AKI after CPB as a consequence of renal tubular damage which affected upstream glomerular filtration due to congestion.…”