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Review: Renin-angiotensin-aldosterone system intervention in the cardiometabolic syndrome and cardio-renal protection

Division of Nephrology, Department of Internal Medicine, University of Missouri Health Sciences Center, One Hospital Dr., MA436, DC 043.0, Columbia MO 65212, whaleyconnella{at}health.missouri.edu

Brian S. Pavey

University of Missouri-Columbia School of Medicine, Departments of Medicine, Physiology, and Pharmacology, Divisions of Endocrinology and Nephrology, Harry S Truman VA Medical Center

Kunal Chaudhary

University of Missouri-Columbia School of Medicine, Departments of Medicine, Physiology, and Pharmacology, Divisions of Endocrinology and Nephrology, Harry S Truman VA Medical Center

Georges Saab

University of Missouri-Columbia School of Medicine, Departments of Medicine, Physiology, and Pharmacology, Divisions of Endocrinology and Nephrology, Harry S Truman VA Medical Center

James R. Sowers

University of Missouri-Columbia School of Medicine, Departments of Medicine, Physiology, and Pharmacology, Divisions of Endocrinology and Nephrology, Harry S Truman VA Medical Center

The metabolic syndrome, also known as the cardiometabolic syndrome (CMS), is a state of metabolic and vascular dysregulation that is associated with activation of the renin-angiotensin-aldosterone system (RAAS). Clinical components of the CMS include central or visceral obesity, hypertension (HTN), dyslipidemia, insulin resistance/hyperinsulinemia, and microalbuminuria that collectively convey increases in oxidative stress, inflammation, and subsequent endothelial dysfunction. The cardio-renal inflammation and oxidative stress enhanced in the CMS increases the risk for cardiovascular disease (CVD) and renal disease end-points such as stroke, congestive heart failure, and chronic kidney disease (CKD). The development of proteinuria is known to herald progressive kidney disease (e.g. CKD) and both are now well accepted as CVD risk factors. Evidence suggests a role for visceral obesity, insulin resistance/hyperinsulinemia, HTN, and other components of the CMS lead to an increased risk for proteinuria and progressive loss of renal function. Intervention with agents that block the RAAS (e.g. ACE inhibitors and Angiotensin type 1 receptor blockers) have been shown to reduce proteinuria, CKD progression, and CVD events. Herein, we will examine the relationship between RAAS intervention and reductions in CKD and CVD events.

Key Words: cardiometabolic syndrome • chronic kidney disease • cardiovascular disease • microalbuminuria.

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