Kidney injury molecule-1 in renal disease

被引:113
|
作者
Waanders, Femke [1 ]
van Timmeren, Mirjan M. [1 ]
Stegeman, Coen A. [1 ]
Bakker, Stephan J. L. [1 ]
van Goor, Harry [1 ]
机构
[1] Univ Groningen, Kidney Ctr, Univ Med Ctr Groningen, NL-9700 RB Groningen, Netherlands
来源
JOURNAL OF PATHOLOGY | 2010年 / 220卷 / 01期
关键词
kidney injury molecule-1; interstitial renal damage; proteinuria; tubular cell injury; biomarker; tubular damage marker; DIETARY-SODIUM RESTRICTION; LONG-TERM PROGNOSIS; POST-HOC ANALYSIS; T-CELL IG; URINARY BIOMARKERS; ACE-INHIBITION; BRAIN-DEATH; RECEPTOR; KIM-1; EXPRESSION;
D O I
10.1002/path.2642
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Kidney injury molecule-1 (KIM-1) is a marker for renal proximal tubular damage, the hallmark of virtually all proteinuric, toxic and ischaemic kidney diseases. KIM-1 has gained increasing interest because of its possible pathophysiological role in modulating tubular damage and repair. In this respect, it is interesting that the best biomarkers often turn out to be important in modulation of damage and some even become therapeutic targets. The emphasis of this review is on structural and biochemical aspects of KIM-1, its expression pattern and its pathophysiological role in renal disease. We also discuss the prognostic impact of KIM-1 in relation to urinary protein excretion. Glomerular (proteinuria) and interstitial markers (KIM-1) might have independent prognostic impact and so may provide independent treatment targets. Finally, the potential of KIM-1 as biomarker of renal damage, as a predictor of renal function decline and its perspectives for monitoring therapy response, are discussed. Copyright (C) 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
引用
收藏
页码:7 / 16
页数:10
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