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NDT Advance Access originally published online on June 7, 2007
Nephrology Dialysis Transplantation 2007 22(9):2435-2439; doi:10.1093/ndt/gfm363
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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

Direct renin inhibitors: the dawn of a new era, or just a variation on a theme?

Liviu Segall1, Adrian Covic1 and David J. A. Goldsmith2

1Nephrology, Dialysis and Renal Transplantation Center, ‘C. I. Parhon’ University Hospital, B-dul Carol I No. 50, Iasi 700503, Romania and 2Renal Unit, Guy's Hospital, London SE1 9RT, UK

Correspondence and offprint requests to: Dr Liviu Segall, MD, Nephrology, Dialysis and Renal Transplantation Center, ‘C. I. Parhon’ University Hospital, B-dul Carol I No. 50, Iasi 700503, Romania. Email: livsegall@yahoo.com

Keywords: chronic kidney disease; direct renin inhibitors; renin-angiotensin-aldosterone system

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



   Renin-angiotensin-aldosterone system (RAAS) inhibitors in chronic kidney disease (CKD): benefits and limitations
 
Numerous studies have demonstrated that the renin-angiotensin-aldosterone system (RAAS) plays an important role in the progression of chronic kidney disease (CKD). Angiotensin (Ang) II generates intrarenal haemodynamic and inflammatory changes that promote proteinuria, growth of glomerular and tubular cells, inhibition of NO synthesis, stimulation of extracellular matrix synthesis and induction of chemokines, reactive oxygen species and apoptosis [1]. In addition, in animal models of renal diseases, aldosterone is also involved in endothelial dysfunction, inflammation, proteinuria and fibrosis [2]. In clinical trials, treatment with angiotensin-converting enzyme (ACE) inhibitors and Ang II AT1 receptor blockers (ARBs) was proved to slow down the evolution of both diabetic and non-diabetic nephropathies and, therefore, it is currently regarded as the cornerstone of what we call ‘nephroprotection’.

A controversial issue is whether these agents are superior to other antihypertensive drugs in terms of nephroprotection—in other words, do they possess so-called ‘pleiotropic’ effects? . . . [Full Text of this Article]



   Combination therapy: more effective, more risks
 


   Direct renin inhibition: an ‘old–new’ strategy of RAAS blockade
 


   Better renoprotection with renin inhibitors?
 


   Conclusion
 

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