Assessment of urinary kidney injury molecule-1 and interleukin-18 in the early post-burn period to predict acute kidney injury for various degrees of burn injury

Abstract

BackgroundBurn patients with AKI have a higher mortality, rapid diagnosis and early treatment of AKI are necessary. Recent studies have demonstrated that urinary KIM-1 and IL-18 are potential biomarkers of early-stage AKI, however, changes in urinary KIM-1 and IL-18 levels are unclear in patients with burns. The aim of our study was to determine whether combined KIM-1 and IL-18 are more sensitive than traditional markers in detecting kidney injury in patients with burns.MethodsNinety-five burn patients hospitalized at the Burns and Plastic Surgery Center of our hospital from April 2013 to September 2013 were enrolled into this prospective study and divided into mild- (n = 37), moderate- (n = 30) and severe-burn groups (n = 28) by burn injury surface area. In the moderate- and severe-burn groups, patients were subcategorized to either the acute kidney injury (AKI) group, in which serum creatinine (Scr) increased to ≥26.5 μmol/L within 48 h, or the non-AKI group. Fifteen healthy subjects were selected as a control group. Blood specimens were collected to determine blood urea nitrogen (BUN), Scr, and other biochemical indicators. Urine samples collected at admission and 48 h after admission were analyzed for KIM-1 and IL-18. Correlations among urinary KIM-1 and IL-18, burn degree, and clinical biochemical indicators were investigated.ResultsAKI occurred in 11.2 % of burn patients (none in the mild-burn group). AKI developed 48 h after admission in 10.0 % of the moderate- and 28.6 % of the severe-burn groups. Urinary KIM-1 concentration in the moderate- and severe-burn groups was significantly higher than that in the control group; urinary IL-18 concentrations did not differ significantly among the burn and control groups. The AKI group had significantly higher concentrations of urinary KIM-1 and IL-18 than the non-AKI group, both at admission (p = 0.001 and p < 0.001, respectively) and 48 h later (p = 0.001 and p < 0.001, respectively). Both urinary KIM-1 and IL-18 increased before Scr. Receiver operating-curve (ROC) analysis demonstrated that KIM-1 combined with IL-18 predicted AKI with 72.7 % sensitivity and 92.8 % specificity. The area under the ROC curve was 0.904.ConclusionsOur results suggest that urinary KIM-1 and IL-18 may be used as early, sensitive indicators of AKI in patients with burns of varying degrees and provide clinical clues that can be used in early prevention of AKI.

Establishment of Novel Urinary Kidney Disease New Biomarkers and Therapeutic Effect of Methanol Fraction of Terminalia Arjuna on Acetaminophen Induced Kidney Disease in Rats

“…SOD, catalase, MDA level of kidney tissue measured in UV-VIS Spectrophotometer by standard protocol [9,15,16]. IL-18 [17,18], KIM-1 [18,19], and cystatin-C [20] were measured by commercially available standard kit with standard protocol for kit literature by an ELISA plate reader.…”

Renal Replacement Therapy for Burn Patients: A Systematic Review and Meta-Analysis

“…A total of 12 studies could not be used for analysis of the prevalence of RRT, seven of which only reported on RRT patients (11,18,21,37,40,43,45), four of which were RCT studies (9, 10, 51, 52), and the remaining one of which were historical controls (44). Most of the 58 studies (41/60) were retrospective cohort studies, but 12 were prospective cohort studies (7,35,39,41,43,46,47,50,57,58,64,65), and 5 RCT studies (9, 10, 51, 52, 56). Moreover, we analysed the results of 41 studies that reported RRT mortality in burn patients ( Table S2).…”

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

“…ACCEPTED MANUSCRIPT 22 prevented the expected increase in serum creatinine after HS [109]. More recently, several studies have examined this p38 pathway even further while simultaneously elucidating additional molecular mechanisms.…”

“…Severe traumatic injuries result in an influx of pro-inflammatory markers (e.g., cytokines, other signaling molecules) that have the potential to supplement clinical data to predict AKI and/or patient outcomes [21][22][23]. In trauma patients who initially survive their injuries, increased plasma levels of the cytokines interleukin-1 (IL-1), IL-6, IL-8, and monocyte chemoattractant protein 1 (MCP1) within the first 24 hours of admittance were associated with AKI occurrence [24].…”