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中性粒细胞在急性肾衰竭中的作用。

The role of neutrophils in acute renal failure.

作者信息

Lauriat S, Linas S L

机构信息

Department of Medicine, University of Colorado Health Sciences Center, and Denver Health Medical Center, 80204, USA.

出版信息

Semin Nephrol. 1998 Sep;18(5):498-504.

PMID:9754602
Abstract

The role of neutrophils in acute renal failure is controversial. Acute renal failure can clearly occur in the absence of neutrophils. However, recent studies using specific neutrophil markers indicate that neutrophils accumulate in postischemic kidneys. Moreover, reperfusion of ischemic kidneys with neutrophils worsens ischemic injury and causes kidney neutrophil retention. Neutrophil retention is dependent on the state of neutrophil activation and the duration of renal ischemia. This interaction could account for the high frequency of acute renal failure in conditions associated with prolonged prerenal asotemia and neutrophil priming such as the adult respiratory distress syndrome, or sepsis. Neutrophil retention is mediated by interaction of neutrophil integrins and endothelial cell ICAM-1 because maneuvers reducing the expression and/or function of these adhesion molecules is protective in experimental models of ischemia. Nitric oxide is a key modulator of neutrophil worsening of ischemic injury because maneuvers that decrease nitric oxide production worsen and those which increase nitric oxide protect ischemic kidneys from neutrophil effects. The clinical significance of neutrophils may relate to the observation that bioincompatible membranes activate complement, and retard recovery from acute renal failure. In conclusion, neutrophils are an important contributor to ischemic acute renal failure. It remains to be determined whether decreasing neutrophil function accelerates recovery in acute renal failure.

摘要

中性粒细胞在急性肾衰竭中的作用存在争议。急性肾衰竭显然可在无中性粒细胞的情况下发生。然而,最近使用特异性中性粒细胞标志物的研究表明,中性粒细胞会在缺血后的肾脏中积聚。此外,用中性粒细胞对缺血肾脏进行再灌注会加重缺血损伤并导致肾脏中性粒细胞滞留。中性粒细胞滞留取决于中性粒细胞的激活状态和肾脏缺血的持续时间。这种相互作用可以解释在与长时间肾前性氮质血症和中性粒细胞预激相关的疾病(如成人呼吸窘迫综合征或脓毒症)中急性肾衰竭的高发生率。中性粒细胞滞留是由中性粒细胞整合素与内皮细胞细胞间黏附分子-1(ICAM-1)的相互作用介导的,因为降低这些黏附分子表达和/或功能的措施在缺血实验模型中具有保护作用。一氧化氮是中性粒细胞加重缺血损伤的关键调节因子,因为减少一氧化氮生成的措施会加重损伤,而增加一氧化氮的措施则可保护缺血肾脏免受中性粒细胞的影响。中性粒细胞的临床意义可能与生物不相容膜激活补体并延缓急性肾衰竭恢复的观察结果有关。总之,中性粒细胞是缺血性急性肾衰竭的重要促成因素。中性粒细胞功能降低是否能加速急性肾衰竭的恢复仍有待确定。

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