Angiotensin receptor blockers: RAAS blockade and renoprotection.
BACKGROUND
Chronic kidney disease (CKD) is an increasingly prevalent public health concern and is associated with a high risk of adverse cardiovascular outcomes. Renal impairment is frequently associated with hypertension and there is compelling evidence of the benefits of antihypertensive therapy for reducing progression of kidney disease. The central role of the renin-angiotensin-aldosterone system (RAAS) in hypertension and renal disease has led to interest in the ability of RAAS-blocking agents to provide benefits beyond blood pressure control.


METHODS
This review explores the mechanisms involved in CKD development, assesses markers of CKD progression, explores the role of the RAAS in renal disease, and examines RAAS blockade as a therapeutic option for renoprotection. For this purpose, a non-systematic literature review was conducted using the Medline database.


RESULTS
Studies in patients with diabetic renal disease have shown that RAAS blockade with angiotensin converting enzyme (ACE)-inhibitors or angiotensin receptor blockers (ARBs) reduces progression of renal disease. Similarly, several studies have demonstrated the benefits of ACE inhibitors in non-diabetic renal disease, although few studies have been conducted with ARBs in this setting. At present, there is little evidence to determine the relative merits of ARBs and ACE inhibitors in terms of clinical outcomes, although ARBs appear to have advantages in terms of renal haemodynamics and measures of renal function.


CONCLUSIONS
The beneficial effects of ARBs, which result from a combination of antihypertensive, haemodynamic, antiproteinuric and pleiotropic mechanisms, provide a strong rationale for considering the use of these agents in the treatment of high-risk patients.
Ruilope
Luis M
LM
Hypertension Unit, Hospital 12 de Octubre, Madrid, Spain. ruilope@ad-hocbox.com
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D003404:Creatinine / Q000652:urine; D003928:Diabetic Nephropathies / Q000150:complications / Q000188:drug therapy; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000517:prevention & control*; D008297:Male; D011379:Prognosis; D011507:Proteinuria / Q000150:complications / Q000503:physiopathology; D016032:Randomized Controlled Trials as Topic; D012084:Renin-Angiotensin System / Q000187:drug effects*; D018570:Risk Assessment; D012720:Severity of Illness Index; D016896:Treatment Outcome
D000806:Angiotensin-Converting Enzyme Inhibitors; D003404:Creatinine