Author's Accepted Manuscript
Introduction George L. Bakris
PII: DOI: Reference:
www.elsevier.com/locate/enganabound S0270-9295(14)00043-6 http://dx.doi.org/10.1016/j.semnephrol.2014.04.001 YSNEP50771
To appear in: Semin Nephrol
Cite this article as: George L. Bakris, Introduction, Semin Nephrol , http://dx.doi.org/10.1016/j.semnephrol.2014.04.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Introduction George L. Bakris Corresponding author:Prof. George L. Bakris The University of Chicago Medicine Department of Medicine ASH Comprehensive Hypertension Center 5841 S. Maryland Avenue, MC1027 Chicago, IL 60637 United States Phone: +1 773-702-7936 Fax: +1 773-834-0486 E-mail: [email protected] Preface for Bakris Aldo issue
The current issue of Seminars in Nephrology focuses on the effects of elevated aldosterone levels on hypertension, cardio-renal function, and other physiological and pathophysiological processes. The focus will be on etiologies associated with secondary elevation in aldosterone not appreciated until the about two to three decades ago. Primary aldosteronism will not be discussed. Elevations in aldosterone, regardless of etiology have long been known to produce elevations in blood pressure and accelerate fibrotic mechanisms within the kidney, heart and vasculature. More recent data demonstrate that increases in aldosterone are implicated as a cause of hypertension in obesity. Research over the past decade has linked increases in aldosterone to the abdominal fat mass of tissue. Adipocyte associated increases in aldosterone production have now been documented by several labs. Reduction in abdominal fat mass following surgical procedures that reduce obesity correlate with marked reductions in aldosterone levels as well as blood pressure. In this issue we review disease states associated with aldosterone excess and not necessarily appreciated by the practicing health care professional. The chapters are designed to present focused information on specific topics as they relate to hypertension, kidney
disease and to a lesser extent heart disease. Given the new information on the role of aldosterone blockade on outcomes in heart disease and the lack of such data on kidney disease progression, clear gaps and opportunities exist to further elucidate the role of aldosterone on disease progression. A key to understanding the relationships between aldosterone and organ injury, including the genesis of hypertension, is a clear grasp of electrolyte balance especially potassium in man. A key paper in this series by Adrogué and Madias presents the integrated physiology of sodium and potassium balance in man and focuses on the role of aldosterone in maintaining this balance. Excess aldosterone has been clearly linked not only to development of elevated blood pressure but more specifically to resistant hypertension. In the first of two specific papers on hypertension and aldosterone, Brent Egan reviews the epidemiology of hypertension and control rates in the general population of the United States as well as in subgroups of those with high cardiovascular risk. This is followed by a contribution of John Bisognano and colleagues that reviews the epidemiology of resistant hypertension in the context of what is currently known. He notes that factors including improper blood pressure measuring techniques, poor medication adherence, and the white coat phenomenon can lead to pseudoresistance, or a false impression of treatment resistance. The effect of abdominal fat and specifically the concept of the adipocyte as an “endocrine” cell has emerged over the past decade. Colleen Flynn reviews the data on aldosterone production and the adipocyte. She presents data that provide an understanding of how the adipocyte may facilitate production of aldosterone. Aldosterone is a key volume hormone and excessive levels are associated with sodium retention and predispose to worsening hypertension and heart failure. Dominic Sica and
colleagues review the physiology of how aldosterone in high levels may exacerbate heart failure symptoms through changes in volume in hypertensive individuals. The importance of aldosterone blockade in cardio-renal conditions such as heart failure or chronic kidney disease in the presence of pre-existing heart disease or diabetes is reviewed by Dr. Lazich and myself. We discuss the important interactions involving aldosterone and approaches to reduce worsening of chronic kidney disease in the presence of heart failure. We further discuss the major limiting factor involved with blocking aldosterone’s effect on organs, i.e. hyperkalemia. We discuss newer approaches to managing potassium homeostasis so that aldosterone effects may be examined. In a separate paper, Bomback and colleagues review the data around aldosterone and chronic kidney disease specifically discussing the effects of aldosterone blockade on proteinuria reduction. While there are no outcome trials of chronic kidney disease progression using aldosterone blockade, there are many cellular and animals studies of the kidney that evaluate the effects of aldosterone in high concentrations. These papers are discussed. The last paper in this series by Ruilope and colleagues presents data on the variety of agents that either directly or indirectly inhibit aldosterone action. They further discuss the resultant effects of such actions on blood pressure and organ preservation.
Introduction George L. Bakris
PII: DOI: Reference:
www.elsevier.com/locate/enganabound S0270-9295(14)00043-6 http://dx.doi.org/10.1016/j.semnephrol.2014.04.001 YSNEP50771
To appear in: Semin Nephrol
Cite this article as: George L. Bakris, Introduction, Semin Nephrol , http://dx.doi.org/10.1016/j.semnephrol.2014.04.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Introduction George L. Bakris Corresponding author:Prof. George L. Bakris The University of Chicago Medicine Department of Medicine ASH Comprehensive Hypertension Center 5841 S. Maryland Avenue, MC1027 Chicago, IL 60637 United States Phone: +1 773-702-7936 Fax: +1 773-834-0486 E-mail: [email protected] Preface for Bakris Aldo issue
The current issue of Seminars in Nephrology focuses on the effects of elevated aldosterone levels on hypertension, cardio-renal function, and other physiological and pathophysiological processes. The focus will be on etiologies associated with secondary elevation in aldosterone not appreciated until the about two to three decades ago. Primary aldosteronism will not be discussed. Elevations in aldosterone, regardless of etiology have long been known to produce elevations in blood pressure and accelerate fibrotic mechanisms within the kidney, heart and vasculature. More recent data demonstrate that increases in aldosterone are implicated as a cause of hypertension in obesity. Research over the past decade has linked increases in aldosterone to the abdominal fat mass of tissue. Adipocyte associated increases in aldosterone production have now been documented by several labs. Reduction in abdominal fat mass following surgical procedures that reduce obesity correlate with marked reductions in aldosterone levels as well as blood pressure. In this issue we review disease states associated with aldosterone excess and not necessarily appreciated by the practicing health care professional. The chapters are designed to present focused information on specific topics as they relate to hypertension, kidney
disease and to a lesser extent heart disease. Given the new information on the role of aldosterone blockade on outcomes in heart disease and the lack of such data on kidney disease progression, clear gaps and opportunities exist to further elucidate the role of aldosterone on disease progression. A key to understanding the relationships between aldosterone and organ injury, including the genesis of hypertension, is a clear grasp of electrolyte balance especially potassium in man. A key paper in this series by Adrogué and Madias presents the integrated physiology of sodium and potassium balance in man and focuses on the role of aldosterone in maintaining this balance. Excess aldosterone has been clearly linked not only to development of elevated blood pressure but more specifically to resistant hypertension. In the first of two specific papers on hypertension and aldosterone, Brent Egan reviews the epidemiology of hypertension and control rates in the general population of the United States as well as in subgroups of those with high cardiovascular risk. This is followed by a contribution of John Bisognano and colleagues that reviews the epidemiology of resistant hypertension in the context of what is currently known. He notes that factors including improper blood pressure measuring techniques, poor medication adherence, and the white coat phenomenon can lead to pseudoresistance, or a false impression of treatment resistance. The effect of abdominal fat and specifically the concept of the adipocyte as an “endocrine” cell has emerged over the past decade. Colleen Flynn reviews the data on aldosterone production and the adipocyte. She presents data that provide an understanding of how the adipocyte may facilitate production of aldosterone. Aldosterone is a key volume hormone and excessive levels are associated with sodium retention and predispose to worsening hypertension and heart failure. Dominic Sica and
colleagues review the physiology of how aldosterone in high levels may exacerbate heart failure symptoms through changes in volume in hypertensive individuals. The importance of aldosterone blockade in cardio-renal conditions such as heart failure or chronic kidney disease in the presence of pre-existing heart disease or diabetes is reviewed by Dr. Lazich and myself. We discuss the important interactions involving aldosterone and approaches to reduce worsening of chronic kidney disease in the presence of heart failure. We further discuss the major limiting factor involved with blocking aldosterone’s effect on organs, i.e. hyperkalemia. We discuss newer approaches to managing potassium homeostasis so that aldosterone effects may be examined. In a separate paper, Bomback and colleagues review the data around aldosterone and chronic kidney disease specifically discussing the effects of aldosterone blockade on proteinuria reduction. While there are no outcome trials of chronic kidney disease progression using aldosterone blockade, there are many cellular and animals studies of the kidney that evaluate the effects of aldosterone in high concentrations. These papers are discussed. The last paper in this series by Ruilope and colleagues presents data on the variety of agents that either directly or indirectly inhibit aldosterone action. They further discuss the resultant effects of such actions on blood pressure and organ preservation.
