Renal protective effect of RAAS blockade across the renal continuum, with a review of the efficacy and safety of valsartan

Abstract

Objective:

The purpose of this report is to review key data on the angiotensin receptor blocker (ARB) valsartan, along with data from several pivotal studies with other ARBs and angiotensin-converting enzyme (ACE) inhibitors, to highlight the beneficial class effects of renin–angiotensin–aldosterone system (RAAS) blockade throughout the renal continuum.

Methods:

The selection of articles was based on a search of PubMed for clinical trials published between 1997 (the year in which valsartan was approved for sale in the US) and 2009 that involved valsartan and reported effects on renal function, plus a select range of articles on other agents acting on the RAAS, including key guidance documents issued during this time.

Summary:

Valsartan has been studied extensively and is widely used for the management of hypertension. Data from clinical studies involving valsartan and other ARBs and ACE inhibitors provide evidence of an additional renal protective effect. This renal protection apparently arises from hemodynamic, endothelial, and anti-inflammatory actions.

Limitations:

Given the extent of the available literature on this topic, this review included only a subset of available publications. This report may reflect inherent heterogeneity between patient populations from these studies and also incorporate the limitations of these individual publications. The inclusion of guidance documents from several organizations may have resulted in apparent minor conflicts in the approaches of the different groups.

Key words::

• Angiotensin-converting enzyme inhibitor
• Angiotensin receptor blocker
• Kidney disease
• RAAS blockade
• Renal protection

Transparency

Declaration of funding

Novartis Pharma AG, Basel, Switzerland provided funding for the editorial support in the development of this article.

Declaration of financial/other relationships

F.L. has disclosed that he is on the advisory board for Novartis. B.F.P. has disclosed that he has received speaker honoraria from Novartis. N.K. has no disclosure. T.E. has disclosed that he is a member of the advisory board of the Renin Academy in Turkey and has received honoraria from Novartis for this paper.

Some peer reviewers receive honoraria from CMRO for their review work. The peer reviewers of this paper have disclosed that they have no relevant financial relationships.

Acknowledgment

The authors acknowledge Oxford PharmaGenesis, Inc. for their editorial support with the development of this manuscript.