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移植而非透析可纠正氮质血症依赖性的中性粒细胞氧化爆发启动。

Transplantation, not dialysis, corrects azotemia-dependent priming of the neutrophil oxidative burst.

作者信息

Klein J B, McLeish K R, Ward R A

机构信息

Department of Medicine, School of Medicine, University of Louisville, Veterans Affairs Medical Center, KY 40202-1718, USA.

出版信息

Am J Kidney Dis. 1999 Mar;33(3):483-91. doi: 10.1016/s0272-6386(99)70185-x.

DOI:10.1016/s0272-6386(99)70185-x
PMID:10070912
Abstract

The oxidative burst of neutrophils from patients with renal failure before the initiation of dialysis is primed for an enhanced response after stimulation by phagocytosis or chemoattractants. This study shows that phagocytosis-stimulated oxidative burst activity remains primed in patients treated with both high-efficiency hemodialysis and continuous ambulatory peritoneal dialysis (CAPD), but it is normal in patients with a functioning renal transplant. Incubation of normal neutrophils or HL-60 granulocytes in azotemic plasma results in increased resting and phagocytosis-stimulated H2O2 production, which is rapidly reversible on removal of the plasma. Priming of the oxidative burst by azotemic plasma is independent of changes in opsonization and phagocytosis and does not require protein synthesis. These results suggest that azotemic plasma contains a substance or substances capable of reversibly priming oxidative burst activity in neutrophils and neutrophil-like cell lines. The Inability of high-efficiency hemodialysis and CAPD to normalize oxidative burst activity suggests that this substance is of higher molecular weight.

摘要

在开始透析前,肾衰竭患者中性粒细胞的氧化爆发在受到吞噬作用或趋化因子刺激后会引发增强反应。本研究表明,接受高效血液透析和持续性非卧床腹膜透析(CAPD)治疗的患者,吞噬作用刺激的氧化爆发活性仍处于引发状态,但肾移植功能正常的患者则正常。将正常中性粒细胞或HL-60粒细胞在氮质血症血浆中孵育会导致静息和吞噬作用刺激的过氧化氢生成增加,去除血浆后这种增加可迅速逆转。氮质血症血浆引发氧化爆发与调理作用和吞噬作用的变化无关,且不需要蛋白质合成。这些结果表明,氮质血症血浆含有一种或多种能够可逆地引发中性粒细胞和类中性粒细胞系氧化爆发活性的物质。高效血液透析和CAPD无法使氧化爆发活性恢复正常,这表明该物质分子量较高。

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