Distant-organ changes after acute kidney injury

被引:54
作者
Feltes, Carolyn M.
Van Eyk, Jennifer
Rabb, Hamid
机构
[1] Departments of Anesthesia and Critical Care Medicine, and Medicine, Johns Hopkins University School of Medicine, Baltimore, MD
[2] Ross 965, Johns Hopkins Hospital, Baltimore, MD 21205
来源
NEPHRON PHYSIOLOGY | 2008年 / 109卷 / 04期
关键词
D O I
10.1159/000142940
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Acute kidney injury (AKI) contributes significantly to morbidity and mortality in both adults and children. While clinical data suggest that AKI contributes to and exacerbates multi-organ failure, the physiologic and molecular mechanisms responsible for these interactions were previously unknown. New data linking AKI with distant-organ dysfunction includes evidence that inflammatory cascades are abnormal after organ injury. Leukocyte trafficking, cytokine expression, cell adhesion-molecule expression and membrane ion and water-channel expression in distant organs are deranged after kidney injury. The responses to oxidative stress after AKI are also altered, suggesting complex mechanisms of crosstalk between the injured kidney and distant organs. Novel methodologies, including genomics and proteomics, are now being employed to unravel interorgan communication to accelerate clinically meaningful discovery for this serious disease. Copyright (c) 2008 S. Karger AG, Basel.
引用
收藏
页码:P80 / P84
页数:5
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