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(Hypertension. 2008;51:15.)
© 2008 American Heart Association, Inc.

Brief Reviews

Interpretation of Plasma Renin Concentration in Patients Receiving Aliskiren Therapy

From the St Vincent’s Institute of Medical Research and the Department of Medicine, University of Melbourne, St Vincent’s Hospital, Fitzroy, Victoria, Australia.

Correspondence to Duncan J. Campbell, St Vincent’s Institute of Medical Research, 41 Victoria Parade, Fitzroy, Victoria 3065, Australia. E-mail dcampbell@svi.edu.au

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

	Introduction

 
Aliskiren (Tekturna or Rasilez) is an orally active renin inhibitor approved for the treatment of hypertension.¹ As with inhibition of the renin-angiotensin system by angiotensin-converting enzyme inhibitors or type 1 angiotensin II (Ang II) receptor blockers, aliskiren therapy is accompanied by a reactive rise in plasma renin concentration, although in contrast to angiotensin-converting enzyme inhibitor and angiotensin receptor blocker therapy, aliskiren reduces enzymatic plasma renin activity (PRA). A direct comparison of aliskiren and angiotensin receptor blocker therapies in hypertensive patients showed differences in the magnitude of the reactive renin response.^2,3 In 1 study, 300 mg/d of aliskiren and 320 mg/d of valsartan were similarly hypotensive, whereas plasma renin concentration was 2-fold higher during aliskiren therapy.³ In a second study, 150 mg/d of aliskiren and 150 mg/d of irbesartan were similarly hypotensive, whereas plasma renin concentration was 1.4-fold higher during aliskiren therapy.^2,4 Moreover, the renin response to 300 mg of aliskiren was 1.6-fold higher than the response to 320 mg of valsartan in sodium-replete normotensive volunteers.⁵ Sealey and Laragh⁶ proposed that the exaggerated renin response may limit aliskiren’s ability to reduce blood pressure by counteracting the effect of renin inhibition on Ang II levels and may thereby account for the failure of 600 mg of aliskiren to reduce blood pressure at >300 mg of aliskiren. They also proposed the renin response to aliskiren therapy may paradoxically increase blood pressure in patients with a highly reactive renin concentration (renovascular, advanced, and malignant hypertension).⁶ Another concern expressed by several authors was the possible . . . [Full Text of this Article]

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