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NDT Advance Access published online on September 21, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm393
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Treatment targets in renal fibrosis

Peter Boor1,2, Katarína Sebeková2, Tammo Ostendorf1 and Jürgen Floege1

1Division of Nephrology, RWTH University of Aachen, Aachen, Germany and 2Department of Clinical and Experimental Pharmacotherapy, Slovak Medical University, Bratislava, Slovakia

Correspondence and offprint requests to: Peter Boor, MD, Division of Nephrology, RWTH University of Aachen, Pauwelsstr. 30, 52074 Aachen, Germany. Email: boor@email.cz

Keywords: animal models; kidney scarring; progressive renal disease; treatment options

The first 150 words of the full text of this article appear below.



   Introduction
 
Renal fibrosis is the principal process underlying the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD). It is a relatively uniform response involving glomerulosclerosis, tubulointerstitial fibrosis and changes in renal vasculature (loss of glomerular and peritubular capillaries) (Figure 1). Of these, tubulointerstitial fibrosis has evolved as the most consistent predictor of an irreversible loss of renal function and progression to ESRD [1].


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  		Fig. 1. Severe tubulointerstitial fibrosis in an experimental rat model of progressive mesangioproliferative glomerulonephritis on day 100 after disease induction. The renal cortical section stained with periodic acid-Schiff (PAS) shows typical tubulointerstitial damage: accumulation of extracellular matrix (*), tubular atrophy (**) and inflammatory infiltrates (***). Glomerular damage is apparent as glomerulosclerosis (arrow) and proteinuria (double arrow). Magnification: 100x.

 
Mechanisms contributing to tubulointerstitial injury and tubular atrophy include glomerular proteinuria, chronic hypoxia, misdirected glomerular ultrafiltration, tubular protein leakage and direct toxic insults . . . [Full Text of this Article]

Renin–angiotensin–aldosterone (RAAS) and kallikrein–kinin system
Endothelin, sympathic nerve system
Environmental factors and metabolic syndrome
Immunosuppressive agents
Turnover and composition of the extracellular matrix
Complement system
Cytokines
Chemokines
TGF-ß, TGF-ß signalling molecules, p38 MAPK, bone morphogenic protein-7 (BMP-7)
Hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF; CCN2)
Vascular endothelial growth factor (VEGF)
Platelet-derived growth factor (PDGF)
Other growth factors
Nitric oxide, NF-{kappa}B and Rho/Rho kinase
Stem cells
Other treatment targets and approaches


   Conclusions
 

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