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目的观察持续性肾脏替代疗法(CRRT)对重症急性胰腺炎(SAP)相关性急性肾损伤(APAKI)的防治效果。方法选择禹州市人民医院和郑州大学第一附属医院确诊的86例SAP患者,随机分为CRRT组和对照组各43例,两组均常规SAP治疗,CRRT组加用CRRT治疗。检测血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、内毒素(ET)、血清尿素氮(BUN)、肌酐(SCr)、尿量、尿比重等,记录发生APAKI的时间、人次和严重程度。结果 CRRT组和对照组10 d内APAKI累计发生概率分别是32.6%和53.5%(Kaplan-Meier法),χ2=4.241,P=0.039。对照组APAKI偏向于较严重(Ⅲ期)的可能性是CRRT组的3.97倍(e1.311≈3.709 878),χ2=3.456,P=0.063。治疗后3、7 d CRRT组TNF-α、IL-6和ET较治疗前降低(P<0.01);对照组各指标较治疗前升高(P<0.01);组间比较差异有统计学意义(P<0.01)。治疗后3、7 d对照组BUN和SCr有升高趋势(P<0.05),CRRT组比治疗前降低(P<0.05或<0.01),组间比较差异有统计学意义(P<0.01)。治疗后两组尿量增加(P<0.05),以CRRT组增加更明显,与对照组相比差异有统计学意义(P<0.01)。治疗后3、7d对照组尿比重标准差值小于CRRT组(P<0.05)。结论 SAP患者肾功能损害明显,CRRT治疗能显著减少APAKI的发生率,减轻肾功能损害程度,清除炎症介质,改善患者的预后。
Objective To observe the effect of continuous renal replacement therapy (CRRT) on the prevention and treatment of severe acute pancreatitis (SAP) -related acute renal injury (APAKI). Methods Eighty-six SAP patients diagnosed by Yuzhou People’s Hospital and the First Affiliated Hospital of Zhengzhou University were randomly divided into CRRT group and control group, 43 cases in each group. Both groups were treated with conventional SAP and CRRT combined with CRRT. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), endotoxin (ET), serum urea nitrogen (BUN), creatinine (SCr), urine output and urine specific gravity APAKI occurred time, the number and severity. Results The cumulative incidence of APAKI in CRRT group and control group within 10 days was 32.6% and 53.5% (Kaplan-Meier method), χ2 = 4.241, P = 0.039. The probability of APAKI being more severe in the control group (stage Ⅲ) was 3.97 times (e1.311≈3.709 878), χ2 = 3.456 and P = 0.063 in CRRT group. The levels of TNF-α, IL-6 and ET in CRRT group at 3 and 7 days after treatment were significantly lower than those before treatment (P <0.01), and those in control group were significantly higher than those before treatment (P0.01). There was significant difference between the two groups (P <0.01). The levels of BUN and SCr increased in the control group (P <0.05) at 3 and 7 days after treatment, but decreased in the CRRT group (P <0.05 or <0.01). There was significant difference between the two groups (P <0.01). After treatment, the urinary output increased in both groups (P <0.05), and increased more significantly in CRRT group compared with the control group (P <0.01). The standard deviation of urinary specific gravity of the control group was less than that of the CRRT group 3 and 7 days after treatment (P <0.05). Conclusion In patients with SAP, renal dysfunction is obvious. CRRT treatment can significantly reduce the incidence of APAKI, reduce the degree of renal dysfunction, clear the inflammatory mediators and improve the prognosis of patients.