期刊
PEDIATRIC NEPHROLOGY
卷 27, 期 6, 页码 901-909出版社
SPRINGER
DOI: 10.1007/s00467-011-1992-9
关键词
Fibrosis; Inflammation; Hypoxia; Proteinuria
资金
- National Institute of Diabetes, Digestive and Kidney Diseases [R01 DK049362, R01 DK075663]
In chronic kidney disease (CKD), once injury from any number of disease processes reaches a threshold, there follows an apparently irreversible course toward decline in kidney function. The tubulointerstitium may play a key role in this common progression pathway. Direct injury, high metabolic demands, or stimuli from various other forms of renal dysfunction activate tubular cells. These, in turn, interact with interstitial tissue elements and inflammatory cells, causing further pathologic changes in the renal parenchyma. The tissue response to these changes thus generates a feed-forward loop of kidney injury and progressive loss of function. This article reviews the mechanisms of this negative cycle mediating CKD.
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