Value of early lactate level in predicting progression of acute kidney injury in patients with extremely severe burns

Abstract

Objective To investigate the value of early lactate levels in predicting the progression of acute kidney injury (AKI) in patients with extremely severe burns. Methods A retrospective case control study was conducted to analyze 30 severe burn patients with early AKI who met the AKI hierarchical diagnostic criteria JP3 (RIFLE) and occurred within 72 hours after injury in the aluminium dust explosion accident in Kunshan City, Jiangsu Province on August 2, 2014. There were 20 males and 10 females, aged 20-50 years [(37.1±7.4)years]. The total area of burn was 75%-100% of total body surface area (TBSA) [(95.5±4.3)% TBSA]. Acute Physiological and Chronic Health Evaluation II (APACHE II) score ranged from 7 to 20 points [(13.0±2.7)points]. According to the progression of renal injury within one week after injury, the patients were divided into aggravation group and non-aggravation group, with 15 patients in each group. Laboratory examinations upon admission such as white blood cell (WBC), platelet, and plasma albumin, medical treatments during the first week after burn injury and 30-day mortality were compared between the two groups. The blood lactic acid, urea nitrogen, creatinine concentration and crinetime kinase in 72 hours after injury were compared between the two groups. The receiver operative characteristic (ROC) curve of early blood lactic acid, blood urea nitrogen, creatinine concentration and crinetime kinase in patients with early AKI after injury was drawn to evaluate its predictive effect on early AKI aggravation in patients with severe burn. Results The plasma albumin concentration of patients in the aggravation group was higher than that in the non-aggravation group on admission to ICU (P 0.05). In the aggravation group, the blood lactate concentration at 24 and 48 hours after injury did not change significantly compared with the first detection after injury (P>0.05), but the concentration at 72 hours after injury was significantly lower than the first detection (P 0.05). The first blood lactate concentration in the aggravation group was significantly higher than that in the non-aggravation group (P 0.05). The blood urea nitrogen concentration of patients in the early AKI aggravation group was higher than that in non-aggravation group on admission (P 0.05). The serumn creatine and creatine kinase concentrations of patients in the aggravation group were higher than those in non-aggravation group 24, 48, and 72 hours after burn injury (P 0.05). The total area under ROC curve of first blood lactic acid, blood urea nitrogen, creatinine and crinetine kinase in early AKI patients were 0.872 (95%CI 0.703-1.000, P 0.05), 0.411 (95%CI 0.143-0.679, P>0.05) and 0.656 (95%CI 0.400-0.911, P>0.05). The optimum threshold for the first blood lactate concentration after injury was 3.5 mmol/L. The sensitivity and specificity for predicting early AKI exacerbation were 100% and 72.7%, respectively. The 30-day mortality rate in the aggravation group was significantly higher than that in the non-aggravation group (P<0.05). Conclusion The first blood lactate concentration in patients with severe burn is an early predictor of AKI aggravation, and its early predictive value is better than that of routine indicators such as serum creatinine blood urea nitrogen and crinetine kinase. Key words: Burns; Acute renal failure; Lactic acid