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Nat Rev Nephrol. 2014 Sep;10(9):493-503. doi: 10.1038/nrneph.2014.114. Epub 2014 Jul 1.

Inflammatory processes in renal fibrosis.

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School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China.
Monash University Department of Medicine, 246 Clayton Road, Clayton, Melbourne, Vic 3168, Australia.
Li Ka Shing Institute of Health Sciences and Department of Medicine &Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong.


Many types of kidney injury induce inflammation as a protective response. However, unresolved inflammation promotes progressive renal fibrosis, which can culminate in end-stage renal disease. Kidney inflammation involves cells of the immune system as well as activation of intrinsic renal cells, with the consequent production and release of profibrotic cytokines and growth factors that drive the fibrotic process. In glomerular diseases, the development of glomerular inflammation precedes interstitial fibrosis; although the mechanisms linking these events are poorly understood, an important role for tubular epithelial cells in mediating this link is gaining support. Data have implicated macrophages in promoting both glomerular and interstitial fibrosis, whereas limited evidence suggests that CD4(+) T cells and mast cells are involved in interstitial fibrosis. However, macrophages can also promote renal repair when the cause of renal injury can be resolved, highlighting their plasticity. Understanding the mechanisms by which inflammation drives renal fibrosis is necessary to facilitate the development of therapeutics to halt the progression of chronic kidney disease.

[Indexed for MEDLINE]

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