This Article Full Text Full Text (PDF) All Versions of this Article: 46/6/1254    most recent 01.HYP.0000190586.07087.cav1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ritz, E. Search for Related Content PubMed PubMed Citation Articles by Ritz, E. Related Collections Related Article

(Hypertension. 2005;46:1254.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Reduction of Microalbuminuria by ß Blockers

Beyond Renin–Angiotensin System Blockade

Eberhard Ritz

From the Department of Nephrology, University of Heidelberg, Germany.

Correspondence to Eberhard Ritz, Department of Nephrology, University of Heidelberg, Heildelberg, Germany.

An extract of the first 250 words of the full text is provided, because this article has no abstract.

After the seminal observations of Mogensen, Parving, and Viberti, it has been increasingly recognized that, in diabetic patients, microalbuminuria predicts not only renal but also cardiovascular risk, and this is true for nondiabetic patients as well. This has led to the recommendation of more widespread testing of urine for microalbuminuria and the use of albuminnuria as a therapeutic target.¹

The mechanism(s) underlying the link between microalbuminuria and cardiovascular risk have remained enigmatic. It is well known that there is crosstalk in the glomerulus between podocytes, the major barrier for the transit of albumin from the capillary to the filtrate, and endothelial cells. Such interaction is mediated mainly by vascular endothelial growth factor.² It has remained enigmatic, however, how albuminuria, that is, podocyte dysfunction, is linked to dysfunction of endothelial cells outside of the glomerulus in the systemic circulation, as reflected by markers of endothelial cell dysfunction/microinflammation³ and by escape of albumin from the circulation into the extravascular space⁴ in microalbuminuric subjects.

In this issue, Bakris et al report the results of a prespecified secondary end point of the GEMINI trial conducted in hypertensive patients with type 2 diabetes.⁵ This part of the study was designed to examine the effects of different ß blockers, that is, metoprolol and carvedilol, on indices of albumin excretion. Following some early studies,⁶ it had been widely accepted that ß blockers have no substantial effect on albuminuria when compared with angiotensin-converting enzyme (ACE) inhibition. The results of the present study go beyond past data and are . . . [Full Text of this Article]

Related Article:

Differential Effects of ß-Blockers on Albuminuria in Patients With Type 2 Diabetes

George L. Bakris, Vivian Fonseca, Richard E. Katholi, Janet B. McGill, Franz Messerli, Robert A. Phillips, Philip Raskin, Jackson T. Wright, Jr, Brian Waterhouse, Mary Ann Lukas, Karen M. Anderson, David S.H. Bell for the GEMINI Investigators
Hypertension 2005 46: 1309-1315. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				H. Kobori, M. Nangaku, L. G. Navar, and A. Nishiyama The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease Pharmacol. Rev., September 1, 2007; 59(3): 251 - 287. [Abstract] [Full Text] [PDF]