Saudi Journal of Kidney Diseases and Transplantation

: 2007  |  Volume : 18  |  Issue : 2  |  Page : 262-

Up-Date on Renal Fibrosis: A Time for Action

E Nigel Wardle 
 London NW1 8JS, United Kingdom

Correspondence Address:
E Nigel Wardle
London NW1 8JS
United Kingdom

How to cite this article:
Wardle E N. Up-Date on Renal Fibrosis: A Time for Action.Saudi J Kidney Dis Transpl 2007;18:262-262

How to cite this URL:
Wardle E N. Up-Date on Renal Fibrosis: A Time for Action. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2022 Nov 29 ];18:262-262
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Full Text

To the Editor:

Readers of my original article [1] may have concluded that on the subject of Fibrosis there is a vast amount of theoretical information, [2] but for the working nephrologists there is only the knowledge that treating patients with a combination of ACE inhibitors and ARBs could lessen fibrosis, or alternatively there is the Et-1 antagonist bosentan, which is not entirely free of side-effects.

However there is encouraging news. It is reported that mycophenolate inhibits mesan­gial cell proliferation and reduces the synthe­sis of extracellular matrix. [3] Then low dose rapamycin has been found to act similarly, albeit by a different mechanism. [4] Finally when type II diabetics are taking gliben­clamide this agent stops extracellular matrix formation by mesangial cells exposed to a high glucose. [5]


1Wardle E N. Renal Fibrosis, Origin and possible Interventions:A Time for Action. Saudi J Kidney Dis Transpl 2006;17{2}:137-48.
2Teng Y, Zeisberg M, Kalluri R. Transcriptional regulation of epithelial­mesenchymal transition. J Clin Invest 2007;117:304-6.
3Ha H, Kim M S, Park J, et al. Mycophenolic acid inhibits mesangial cell activation through p38 MAPkinase inhibition. Life Science 2006;79:1561-7
4Lock H R, Sacks S H, Robson M G. Rapamycin at sub-immunosuppressive levels inhibits mesangial cell proliferation and extracellular matrix production. Am J Physiol Renal Physiol 2007;292:F76-F81.
5Giannico G, Cortes P, Baccora MH, et al. Glibenclamide prevents increased extra­cellular matrix formation induced by a high glucose concentration in mesangial cells. Am J Physiol physiol Renal 2007;292:F57-F65.