Renoprotection of angiotensin receptor blockers: beyond blood pressure lowering

1Institute of Medical Sciences and Division of Nephrology, Hypertension and Metabolism, Tokai University School of Medicine, Kanagawa, Japan and 2Service de Nephrologie, Universite Catholique de Louvain, Brussels, Belgium In pioneering studies, Mogensen [1] and Parving et al. [2] have demonstrated that anti-hypertensive treatment slowed the decline of renal function in hypertensive patients with diabetic nephropathy. These observations were subsequently extended to other types of hypertensive renal diseases. No attention was paid to the type of the utilized anti-hypertensive drug: blood pressure lowering was the main goal. Several clinical studies, mainly but not exclusively in diabetic patients, have subsequently suggested that anti-hypertensive agents inhibiting the renin–angiotensin system (RAS), such as angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs), achieved better renoprotection than other anti-hypertensive drugs [3–7]. Inhibitors of the RAS not only protected renal function, but also lowered proteinuria even at the level of microalbuminuria [6,7]. Microalbuminuria emerged as an important independent risk factor not only for end-stage renal failure but also for cardiovascular disease [8]. As a result, ARBs and ACEIs are now part of the standard treatment of patients with diabetic nephropathy, regardless of the presence of systemic hypertension.