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NDT Advance Access originally published online on October 5, 2006
Nephrology Dialysis Transplantation 2007 22(1):5-8; doi:10.1093/ndt/gfl549
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Secondary rise of albuminuria under AT1-receptor blockade—what is the potential role of aldosterone escape?

Lars Christian Rump

Klinikum der Ruhr-Universität Bochum, Marienhospital Herne, Bochum, Germany

Correspondence and offprint requests to: Prof. Dr L. C. Rump, Klinikum der Ruhr-Universität Bochum, Medizinische Klinik I, Marienhospital Herne, Hölkeskampring 40, 44625 Herne, Germany. Email: christian.rump@ruhr-uni-bochum.de

Keywords: ACE inhibition; albuminuria; aldosterone escape; angiotensin II; AT1-receptor blockade

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



   Introduction
 
Inhibition of the renin–angiotensin system is the recommended standard therapeutic regimen in chronic kidney disease. The reasons for this choice are obvious. On the one hand angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) are almost indispensable to reach target blood pressure in this group of patients [1]. On the other hand they cause blood pressure independent reductions of proteinuria which ameliorates renal disease progression [2]. Moreover, the presence of glomerular proteinuria is indicative for high cardiovascular risk. It is now generally accepted that the antiproteinuric response to inhibitors of the RAS predicts not only progression, but also cardiovascular outcome in chronic renal failure [3]. Those patients with the largest reduction of proteinuria have the greatest cardiovascular benefit. Unfortunately—after an initial decrease—in many patients proteinura rises again under continued ACE inhibitor therapy. Such secondary increase in albuminiuria has even occured in non-renal patients treated . . . [Full Text of this Article]



   Aldosterone and proteinuria
 


   What is known about aldosterone escape under RAS blockade?
 


   Clinical considerations and outlook
 

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