急性肾衰竭患者持续静脉-静脉血液滤过消除肝活性物质的研究。

Kidney international. Supplement Pub Date : 1999-11-01
W Riegel, A Habicht, C Ulrich, H Köhler
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引用次数: 0

摘要

背景:危重患者急性肾功能衰竭(ARF)多为多器官功能衰竭的一部分。因此,肾脏替代疗法对肝脏的影响具有重要的临床意义。我们研究了连续静脉-静脉血液滤过(CVVH)患者超滤液对体外肝细胞的影响。方法:对ARF患者连续使用Multiflow60 (I组)或FH66过滤器(II组)进行CVVH治疗,两组患者在诊断、年龄、性别、实验室参数、肾脏替代治疗等方面具有可比性,但在日利尿、血清水平、血流量等方面存在差异。在更换血液滤器后的前10分钟内收集超滤液。测定HepG2细胞的增殖(溴脱氧尿苷)、活力(乳酸脱氢酶)和急性期蛋白分泌。结果:超滤液对肝细胞功能的影响明显高于对照组。HepG2细胞增殖(I组29.8+/-5.2%比II组48.4+/-6.6%,P < 0.05)和活力(I组78.7+/-2.0%比II组87.6+/-1.7%,P < 0.01)差异有统计学意义。一方面,Multiflow60超滤液显著降低了急性期阴性蛋白转铁蛋白的分泌[13.1+/-0.2 (ng/microg protein)组与ⅱ组5.1+/-0.5 (ng/microg protein), P < 0.01]。另一方面,Multiflow60超滤液显著刺激急性期蛋白α - 1-酸性糖蛋白阳性[I组2.6+/-0.1 (ng/微克蛋白)vs II组1.7+/-0.1 (ng/微克蛋白),P < 0.001]。结论:本研究证实了超滤液中存在肝活性介质。它们具有肝毒性并影响急性期蛋白质代谢。进一步的研究必须阐明两组的不同影响,并分析假定的中介因素。在危重患者中,考虑治疗措施以优化肾脏替代治疗仍然是一项具有挑战性的任务。
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Hepatoactive substances eliminated by continuous venovenous hemofiltration in acute renal failure patients.

Background: Acute renal failure (ARF) in critically ill patients is mostly part of a multi-organ failure. Therefore, the effects of renal replacement therapy on the liver are clinically important. We investigated the effects of ultrafiltrates of patients treated with continuous venovenous hemofiltration (CVVH) on liver cells in vitro.

Methods: Patients with ARF were consecutively treated with CVVH using Multiflow60 (group I) or FH66 filters (group II). They were comparable with respect to diagnosis, age, sex, laboratory parameters, and renal replacement treatment, but were different in daily diuresis, serum levels, and blood flow. Ultrafiltrates were collected within the first 10 minutes after change of hemofilter. Proliferation (bromodeoxyuridine), vitality (lactate dehydrogenase), and acute-phase protein secretion of HepG2 cells were measured.

Results: Ultrafiltrates changed liver cell function significantly compared with medium control. Proliferation (group I 29.8+/-5.2% vs. group II 48.4+/-6.6%, P < 0.05) and vitality (group I 78.7+/-2.0% vs. group II 87.6+/-1.7%, P < 0.01) of HepG2 cells were significantly different. On the one hand, the secretion of the negative acute-phase protein transferrin [group 13.1+/-0.2 (ng/microg protein) vs. group II 5.1+/-0.5 (ng/microg protein), P < 0.01] was significantly reduced by Multiflow60 ultrafiltrates. On the other hand, positive acute-phase protein alpha1-acid glycoprotein was significantly stimulated by Multiflow60 ultrafiltrates [group I 2.6+/-0.1 (ng/microg protein) vs. group II 1.7+/-0.1 (ng/microg protein), P < 0.001].

Conclusion: This study demonstrates hepatoactive mediators in the ultrafiltrates. They are hepatotoxic and influence acute-phase protein metabolism. Further studies have to elucidate the different effects in both groups and the analysis of the putative mediator(s). It remains a challenging task to consider therapeutic measures to optimize renal replacement therapy in critically ill patients.

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