Blood Pressure in Renal Disease: Objectives, Surrogate Markers and TreatmentRobles NR*
Cardiovascular Risk Chair, Universidad de Salamanca, Salamanca, Spain
- *Corresponding Author:
- Nicolás Roberto Robles
Unidad de HTA, Hospital Infanta Cristina
Carretera de Portugal s/n, 06080, Badajoz, Spain
E-mail: [email protected]
Received date: November 30, 2012; Accepted date: December 28, 2012; Published date: December 30, 2012
Citation: Robles NR (2013) Blood Pressure in Renal Disease: Objectives, Surrogate Markers and Treatment. Med Surg Urol S11:002. doi:10.4172/2168-9857.S11-002
Copyright: © 2013 Robles NR. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Despite decades of trials, we still are uncertain as to what level we should lower BP to achieve maximalcardiovascular protection in hypertensive patients. Even more, nowadays the target for reducing blood pressure inrenal disease is under discussion; there is scanty evidence from randomized clinical trials to support a straight bloodpressure control for proteinuric patients.
On the other hand the value of microalbuminuria as surrogate marker of renal disease progression is controversialin hypertensive non diabetic patients. Furthermore, frequently the effects of treatment on glomerular filtration rate themore used and useful test for chronic kidney disease- are opposite in several clinical trials.
The Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension(ACCOMPLISH) trial showed that initial antihypertensive therapy with benazepril plus amlodipine was superior to benazepril plus hydrochlorothiazide in reducing progression of chronic kidney disease as well as cardiovascular morbidityand mortality in renal patients. The renal results of the ACCOMPLISH trial strongly support the recommendation ofusing calcium channel blockers as second antihypertensive agent added to renin-angiotensin axis blocking drugs. Thevalidity of this data and its relationship with the cumulated evidence on the effects of calcium antagonists (especially new calcium channel blockers which reduce proteinuria) on renal disease progression will be discussed.