Mancia Cardiorenal Syndrome

Mechanisms, Risk and Treatment
1. Auflage 2010
ISBN: 978-88-470-1463-3
Verlag: Springer-Verlag
Format: PDF
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 396 Seiten

Chronic kidney disease with a worldwide prevalence of 10% in the general population is emerging as a major public health priority. Renal dysfunction is associated with a high risk for cardiovascular complications. The relationship between renal insufficiency and cardiovascular disease, termed the cardiorenal syndrome exists whether impairment of renal function is a consequence of primary renal parenchymal disease or primary heart disease. Several pathophysiologic mechanisms have been postulated to explain the relationship between renal dysfunction and cardiovascular disease. Recent studies indicate an integrated response of the vascular smooth muscles and glomerular mesangial cells to traditional and uremia related cardiovascular risk factors. Traditional risk factors can incite renal impairment and cardiac damage. As renal function deteriorates, uremia-related risk factors play an increasing role both in reduction in glomerular filtration rate and cardiovascular damage. Several uremia related factors such as uncontrolled hypertension, disturbed glucose insulin metabolism, microalbuminuria, phosphate retention, secondary hyperparathyroidism, myocardial and vascular calcification, hypertensive-uremic cardiomyopathy, inflammation, oxidant injury, and neurohormonal dysregulation have been implicated in the pathogenesis of the cardiorenal syndrome. Recent data suggest that management of the cardiorenal syndrome requires aggressive control of traditional risk factors as well novel approaches to prevent or reverse uremia -related processes. This book provides a comprehensive update analysis of our current understanding of the cardiorenal syndrome including epidemiology, pathophysiologic mechanisms, and therapeutic approaches.

Autoren/Hrsg.

Mancia, Giuseppe

Inhaltsverzeichnis

1;Preface;5
2;Table of Contents;6
3;List of Contributors;10
4;Section I Chronic Kidney Disease and Cardiovascular Disease Interrelationships;15
4.1;1 Links between Chronic Kidney Disease and Cardiovascular Disease: A Bidirectional Relationship ;16
4.1.1;1.1 Introduction;16
4.1.2;1.2 Definition;17
4.1.3;1.3 Chronic Kidney Disease as a Promoter of Cardiovascular Disease;17
4.1.3.1;1.3.1 Epidemiology;17
4.1.3.2;1.3.2 Pathophysiologic Mechanisms;18
4.1.3.2.1;1.3.2.1 Atherosclerosis;19
4.1.3.2.2;1.3.2.2 Arteriosclerosis;20
4.1.3.2.3;1.3.2.3 Endothelial Dysfunction;21
4.1.3.2.4;1.3.2.4 Uremia-Related CVD;22
4.1.3.3;1.3.3 Course of CVD in CKD;22
4.1.4;1.4 CVD in Kidney Transplant Recipients;22
4.1.5;1.5 Cardiac Disease as a Promoter of Kidney Dysfunction;23
4.1.6;1.6 Conclusions;24
4.1.7;References;25
4.2;2 Cardiorenal versus Renocardiac Syndrome;28
4.2.1;2.1 Introduction;28
4.2.2;2.2 Heart Failure as a Cause of Kidney Failure (Cardiorenal Syndrome);29
4.2.2.1;2.2.1 Ventricular Dilation in Congestive Heart Failure;29
4.2.2.2;2.2.2 Left Ventricular Mass Index and Congestive Heart Failure;31
4.2.2.3;2.2.3 Blunted Atrial–Renal Reflexes and Chronic Heart Failure;31
4.2.2.4;2.2.4 Neurohormones and Chronic Heart Failure;31
4.2.2.4.1;2.2.4.1 Renin–Angiotensin–Aldosterone System;31
4.2.2.4.2;2.2.4.2 Sympathetic Nervous System;33
4.2.2.4.3;2.2.4.3 Arginine Vasopressin;33
4.2.2.5;2.2.5 Cardiorenal Intersection in Heart Failure;34
4.2.3;2.3 Chronic Kidney Disease as a Pathogenic Factor for Cardiovascular Disease (Renocardiac Syndrome);36
4.2.3.1;2.3.1 Accelerated Atherosclerosis in Chronic Kidney Disease;36
4.2.3.2;2.3.2 Role of Traditional Risk Factors and Cardiovascular Outcomes in Patients with Chronic Kidney Disease;37
4.2.3.2.1;2.3.2.1 Hypertension;37
4.2.3.2.2;2.3.2.2 Diabetes Mellitus;38
4.2.3.2.3;2.3.2.3 Dyslipidemia;39
4.2.3.2.4;2.3.3Novel Risk Factors in Cardiovascular Disease Progression in Patients with ChronicKidney Disease;40
4.2.3.2.4.1;2.3.3.1 Anemia;40
4.2.3.2.4.2;2.3.3.2 Oxidative Stress;41
4.2.3.2.4.3;2.3.3.3 Endothelial Dysfunction;41
4.2.3.2.4.4;2.3.3.4 Lipoprotein (a);41
4.2.3.2.4.5;2.3.3.5 Hyperhomocysteinemia;42
4.2.3.2.4.6;2.3.3.6Inflammation and High-Sensitivity C-Reactive Protein;42
4.2.3.2.4.7;2.3.3.7 Accelerated Coronary Calcification;43
4.2.3.2.4.8;2.3.3.8 Other Novel Risk Factors;43
4.2.4;2.4 Chronic Kidney Disease and Valvular Heart Disease;43
4.2.5;2.5 Chronic Kidney Disease and Arrhythmias;44
4.2.6;2.6 Conclusions;44
4.2.7;References;45
5;Section IICrosstalk between the CardiovascularSystem and the Kidney;48
5.1;3 Non-Pressure-Related DeleteriousEffects of Excessive Dietary Sodium;49
5.1.1;3.1 Introduction;49
5.1.2;3.2 Measurement of 24-Hour Urinary Sodium is the Gold Standard for Estimating Sodium Intake;50
5.1.3;3.3 Influence of Sodium Intake on Subclinical Organ Damage;50
5.1.4;3.4 Does the Influence of Dietary Sodium on Target-Organ Damage Translate into a Difference in Risk?;52
5.1.5;3.5 Studies on the Effect of Salt Restriction;52
5.1.6;3.6 Is Reduction in Dietary Sodium Associated with a Reduction in Cardiovascular Risk?;53
5.1.7;3.7 Evidences in Favor of a Direct Effect of Dietary Sodium;53
5.1.8;3.8 Mechanism(s) Involved in the Deleterious Effect of Salt;54
5.1.9;3.9 Conclusions;56
5.1.10;References;57
5.2;4 Regulation of Vascular and Renal Cells by Common Mediators in Health and Disease: Role of the Renin–Angiotens in Systemin the Pathophysiology of Hypertension and Cardiovascular Disease;60
5.2.1;4.1 Renin–Angiotensin System in Vascular and Renal Diseases: From the Classic View to the New and Complex System;61
5.2.2;4.2 Pharmacological Blockade of Renin–Angiotensin System in Vascular and Renal Diseases;63
5.2.3;4.3 Common Responses to Angiotensin II in Vascular and Renal Diseases: Modulation of Fibrosis and Inflammation;64
5.2.3.1;4.3.1 Angiotensin II and Cell Growth Regulation in Vascular and Renal Diseases;65
5.2.3.2;4.3.2 AngII Regulates Fibrosis via AT1 receptor: Role of CTGF and Smad Signaling Pathway;65
5.2.3.3;4.3.3 Role of Angiotensin II in the Inflammatory Response in Vascular and Renal Diseases;67
5.2.3.4;4.3.4 Active Role of AngII in Different Steps of Atherosclerosis;70
5.2.4;4.4 Role of Angiotensin Peptides in Vascular and Renal Diseases;70
5.2.4.1;4.4.1 AngIV in Cardiovascular Damage;71
5.2.4.2;4.4.2 Ang-(1–7) in Renal and Cardiovascular Damage;71
5.2.4.3;4.4.3 Conclusions;72
5.2.5;References;73
6;Section III Chronic Kidney Disease as a Risk forCardiovascular Disease;75
6.1;5 Cardiorenal Continuum;76
6.1.1;5.1 Introduction;76
6.1.2;5.2 Cardiovascular Disease Associated with Renal Disease: Evidences Along the Continuum;78
6.1.2.1;5.2.1 Global Therapeutic Approach Focused on Renal Outcomes;84
6.1.3;References;85
6.2;6 Definition and Classification of Stages of Chronic Kidney Disease: Screening for Chronic Kidney Disease;89
6.2.1;6.1 Introduction;89
6.2.2;6.2 Definition of Chronic Kidney Disease;90
6.2.3;6.3 Classification of Chronic Kidney Disease;90
6.2.4;6.4 Chronic Kidney Disease Screening;92
6.2.5;6.5 Conclusions;96
6.2.6;References;96
6.3;7 Cardiovascular Disease Risk Factors in Chronic Kidney Disease: Traditional, Nontraditional, and Uremia-related Threats;98
6.3.1;7.1 Introduction;98
6.3.2;7.2 Epidemiological Considerations;99
6.3.2.1;7.2.1 Difficulties in Describing Causes of Death;99
6.3.2.2;7.2.2 Effects of Changing Demographics and Race on CVD in CKD;100
6.3.2.3;7.2.3 Reverse Epidemiology;100
6.3.3;7.3 Traditional Risk Factors;101
6.3.3.1;7.3.1 Age, Gender, and Smoking;101
6.3.3.2;7.3.2 Diabetes Mellitus;101
6.3.3.3;7.3.3Hypertension;102
6.3.3.4;7.3.4 Insulin Resistance;102
6.3.3.5;7.3.5 Dyslipidemia;102
6.3.4;7.4 Nontraditional and/or Uremia-specific Risk Factors;103
6.3.4.1;7.4.1 Renal Failure Per Se;103
6.3.4.2;7.4.2 Oxidative Stress;103
6.3.4.3;7.4.3 Hyperhomocysteinemia;104
6.3.4.4;7.4.4 Inflammation;105
6.3.4.5;7.4.5 Endothelial dysfunction;106
6.3.4.6;7.4.6 Secondary Hyperparathyroidism and Mineral Metabolism;107
6.3.4.7;7.4.7 Cardiovascular Calcification;107
6.3.4.8;7.4.8 Autonomic Dysfunction;108
6.3.4.9;7.4.9 Anemia;108
6.3.4.10;7.4.10 Hormonal Derangements;108
6.3.5;References;109
6.4;8 Increased Levels of Urinary Albumin: A Cardiovascular Risk Factor and a Target for Treatment;112
6.4.1;8.1Introduction;112
6.4.2;8.2 Definition of Albuminuria;113
6.4.2.1;8.2.1 How Do We Measure Albuminuria?;113
6.4.2.1.1;8.2.1.1 Protein or Albumin?;113
6.4.2.1.2;8.2.1.2 Measurement Technique;114
6.4.2.1.3;8.2.1.3 Urine Collection;114
6.4.2.1.4;8.2.1.4 Fresh or Frozen Sample?;116
6.4.3;8.3 Epidemiology;116
6.4.4;8.4 Pathophysiology;117
6.4.5;8.5 CVD Risk Prediction;117
6.4.6;8.6 Targeting Albuminuria for CVD Risk Protection;119
6.4.7;References;121
6.5;9 Microalbuminuria and Kidney Disease: An Evidence-based Perspective;124
6.5.1;9.1 Introduction;124
6.5.2;9.2 Definition of Microalbuminuria;125
6.5.3;9.3 Prevalence of Microalbuminuria;126
6.5.4;9.4 Pathophysiology of Microalbuminuria;126
6.5.5;9.5 Cardiovascular Risk;127
6.5.5.1;9.5.1 Hypertension;127
6.5.5.2;9.5.2 Hyperinsulinemia;128
6.5.5.3;9.5.3 Endothelial Dysfunction;128
6.5.5.4;9.5.4 Dyslipidemia;129
6.5.5.5;9.5.5 C-reactive Protein;130
6.5.5.6;9.5.6 Genetic Associations;130
6.5.5.7;9.5.7 Vascular Risk Assessment;130
6.5.6;9.6 Prognostic Implications;130
6.5.7;9.7 Chronic Kidney Disease;132
6.5.8;9.8 Therapeutic Intervention and Cardiorenal Disease Risk Reduction;133
6.5.9;9.9 Conclusions;134
6.5.10;References;135
6.6;10 Cardiometabolic Syndrome;138
6.6.1;10.1 Introduction;138
6.6.2;10.2 Definition and Origins of Cardiometabolic Syndrome;139
6.6.3;10.3 Cardiometabolic Syndrome and CKD Risk;141
6.6.3.1;10.3.1 Microalbuminuria;141
6.6.3.2;10.3.2 CKD;141
6.6.4;10.4 Proposed Mechanisms of CKD Risk in Cardiometabolic Syndrome;143
6.6.4.1;10.4.1 Pathologic Findings;144
6.6.4.2;10.4.2 Lipotoxicity;144
6.6.4.3;10.4.3 Inflammation;144
6.6.4.4;10.4.4 Activation of the Renin–Angiotensin System (RAS) Axis;145
6.6.4.5;10.4.5 Obesity and Obesity-Related Hemodynamic Factors;145
6.6.4.6;10.4.6 Hyperuricemia;145
6.6.5;10.5Cardiometabolic Syndrome and CVD Risk;146
6.6.5.1;10.5.1 Studies in the General Population;146
6.6.5.2;10.5.2 Studies in CKD Populations;146
6.6.6;10.6 Implications for CKD and CVD Risk Prediction and Risk Reduction;147
6.6.6.1;10.6.1 Risk Prediction;147
6.6.6.2;10.6.2 Risk Reduction Strategies;148
6.6.7;References;149
6.7;11 Diabetes Mellitus: Is the Presence of Nephropathy Important as a Cardiovascular Risk Factor for Cardiorenal Syndrome?;152
6.7.1;11.1 Introduction;153
6.7.2;11.2 Diabetes Mellitus;153
6.7.2.1;11.2.1 Diabetes and the Kidney;153
6.7.2.2;11.2.2 Diabetes and the Heart;154
6.7.2.3;11.2.3 Micro- and Macroalbuminuria in Diabetes and CVD Risk;154
6.7.3;11.3 CKD and CVD;155
6.7.4;11.4 Pathogenesis;158
6.7.5;11.5 Treatment;159
6.7.6;11.6 Conclusions;160
6.7.7;Reference;161
7;Section IV Spectrum of Cardiovascular Disease in Chronic Kidney Disease;165
7.1;12 Cardiovascular Disease: Coronary Artery Disease and Coronary Artery Calcification;166
7.1.1;12.1 Introduction;166
7.1.2;12.2 Coronary Artery Disease in Chronic Kidney Disease;167
7.1.2.1;12.2.1 Etiology and Pathogenesis of CAD in CKD;167
7.1.2.2;12.2.2 Potential Mechanisms of Accelerated Atherosclerosis in CKD;168
7.1.2.2.1;12.2.2.1 Visceral Adiposity and Atherosclerosis in CKD;168
7.1.2.2.2;12.2.2.2 Serum Vitamin D, Fibroblast Growth Factor-23 and Alkaline Phosphatase;169
7.1.2.2.3;12.2.2.3 Hypertension;170
7.1.2.2.4;12.2.2.4 Dyslipidemia;170
7.1.2.2.5;12.2.2.5 Inflammation and Oxidative Stress;170
7.1.2.3;12.2.3 Clinical Presentation and Diagnosis of CAD in CKD;171
7.1.2.3.1;12.2.3.1 Laboratory Diagnosis of Acute Coronary Syndromes;171
7.1.2.3.2;12.2.3.2 Stress Tests for Diagnosis of Chronic Myocardial Ischemia;171
7.1.2.3.3;12.2.3.3 Electron Beam Computed Tomography;171
7.1.3;12.3 Therapy for CAD in CKD;172
7.1.3.1;12.3.1 Antiplatelet Agents;172
7.1.3.2;12.3.2 Beta Blockers;172
7.1.3.3;12.3.3Angiotensinogen-converting Enzyme (ACE) Inhibitors/AngiotensinReceptor Blockers (ARB);173
7.1.3.4;12.3.4 Lipid-Lowering Therapy;173
7.1.4;12.4 Coronary Revascularization in CKD;174
7.1.5;12.5 Coronary Calcification in CKD;175
7.1.6;References;176
7.2;13 Cardiomyopathy in Chronic Kidney Disease and in End-stage Renal Disease;179
7.2.1;13.1 Introduction;180
7.2.2;13.2 Left Ventricular Mass and Function in Stages 3–5 Chronic Kidney Disease Patients and Dialysis Patients;180
7.2.2.1;13.2.1 Problem of Appropriate Indexing;180
7.2.2.2;13.2.2 Cardiomyopathy in Stages 3–5 Chronic Kidney Disease Patients;181
7.2.2.3;13.2.3 Cardiomyopathy in End-stage Renal Disease Patients;183
7.2.3;13.3 Drug Treatment of Left-Ventricular Disorders in Chronic Kidney Disease and End-stage Renal Disease Patients;186
7.2.4;13.4 Dialysis Treatment Modalities, Implantable Cardioverters, and Cardiac Resynchronization in End-stage Renal Disease Patients with Left-ventricular Systolic Dysfunction;187
7.2.5;13.5Conclusions;188
7.2.6;References;189
7.3;14 Pathophysiological Mechanisms and Prognostic Significance of Renal Functional Impairment in Cardiac Patients;192
7.3.1;14.1 Definition of Cardiorenal Syndrome;193
7.3.2;14.2 Prevalence of Renal Functional Impairment in HF;193
7.3.3;14.3 Pathophysiological Mechanisms;194
7.3.3.1;14.3.1 Complex Mechanisms Involved in ECFV (Dys)regulation in HF;195
7.3.3.2;14.3.2 CRC: Mechanisms Beyond ECFV Regulation;196
7.3.3.2.1;14.3.2.1 RAAS;197
7.3.3.2.2;14.3.2.2 Balance Between NO and ROS;197
7.3.3.2.3;14.3.2.3 Inflammation;197
7.3.3.2.4;14.3.2.4 SNS;197
7.3.3.3;14.3.3 Importance of Central Venous Pressure;198
7.3.3.4;14.3.4 Anemia: The Third Condition of a Deadly Triad?;199
7.3.4;14.4 Prognostic Significance;200
7.3.4.1;14.4.1 Chronic HF;200
7.3.4.2;14.4.2 Acute HF;201
7.3.5;References;203
7.4;15 Stroke;207
7.4.1;15.1 Introduction;207
7.4.2;15.2 Epidemiology;208
7.4.2.1;15.2.1 Gauging Stroke Risk in CKD;208
7.4.3;15.3 Mechanisms of Stroke Occurrence in CKD;208
7.4.3.1;15.3.1 Blood Pressure;208
7.4.3.2;15.3.2 Dyslipidemia;209
7.4.3.3;15.3.3 Anemia;209
7.4.3.4;15.3.4 Proteinuria;209
7.4.4;15.4 Management of Stroke Risk in CKD;211
7.4.4.1;15.4.1 Hypertension;211
7.4.4.2;15.4.2 Dyslipidemia;213
7.4.4.3;15.4.3 Anemia;214
7.4.4.4;15.4.4 Other Targets;214
7.4.5;15.5 Conclusions;215
7.4.6;References;215
8;Section V Mechanisms of Cardiovascular Complications;218
8.1;16 Uremic Toxins;219
8.1.1;16.1 Introduction;219
8.1.2;16.2 Cardiovascular Implications;220
8.1.3;16.3 Classification of Uremic Retention Solutes;220
8.1.3.1;16.3.1 Advanced Glycation End Products;222
8.1.3.2;16.3.2 Advanced Oxidation Protein Products;223
8.1.3.3;16.3.3 Angiogenin – Degranulation-inhibiting Protein I;223
8.1.3.4;16.3.4 Angiotensin II Variants;224
8.1.3.5;16.3.5 Complement Factor D;224
8.1.3.6;16.3.6 p-Cresyl Sulphate;224
8.1.3.7;16.3.7 Cytokines;225
8.1.3.8;16.3.8 Dinucleoside Polyphosphates;225
8.1.3.9;16.3.9 Guanidines;226
8.1.3.10;16.3.10 Homocysteine;226
8.1.3.11;16.3.11 Immunoglobulin Light Chains;227
8.1.3.12;16.3.12 Indoxyl Sulphate;227
8.1.3.13;16.3.13 Leptin;228
8.1.3.14;16.3.14 B2 Microglobulin and AGE-modified B2 Microglobulin;228
8.1.3.15;16.3.15 Oxalic Acid;229
8.1.3.16;16.3.16 Phenylacetic Acid;229
8.1.4;16.4 Conclusions;230
8.1.5;References;231
8.2;17 Endothelial Dysfunction, Nitric OxideBioavailability, and AsymmetricDimethyl Arginine;235
8.2.1;17.1 Introduction;235
8.2.2;17.2 Basic Biochemistry of the NO System;236
8.2.3;17.3 Endothelial Dysfunction: Molecular Mechanisms;237
8.2.4;17.4 Endothelial NOS Activity Modulation and Factors Affecting NO Bioavailability;237
8.2.5;17.5 Biomarkers of Endothelial Function;239
8.2.6;17.6 Endothelial and Renal Dysfunction in Essential Hypertension and in the Aging Kidney;240
8.2.7;17.7 Endogenous Inhibitors of the Nitric Oxide System, CKD, and Cardiorenal Risk;242
8.2.8;17.8 ADMA as a Risk Factor for CKD;242
8.2.9;References;243
8.3;18 Pathophysiologic Link between Atherosclerosis and Nephrosclerosis;245
8.3.1;18.1 Introduction;245
8.3.2;18.2 Lipid Accumulation;246
8.3.3;18.3 Inflammation;247
8.3.4;18.4 Cellular Proliferation;249
8.3.5;18.5Extracellular Matrix Turnover;249
8.3.6;18.6 Thrombosis;251
8.3.7;References;252
8.4;19 Aortic Stiffness, Kidney Disease, and Renal Transplantation;254
8.4.1;19.1 Introduction;254
8.4.2;19.2 Large Artery Damage in Chronic Renal Disease;255
8.4.2.1;19.2.1 Individuals with ESRD;255
8.4.2.2;19.2.2 Individuals with Mild to Moderate Renal Insufficiency;256
8.4.3;19.3 Calcium and Arterial Calcifications;257
8.4.4;19.4 Pulse Pressure, Renal Autoregulation, and End-organ Damage;258
8.4.4.1;19.4.1 Kidney Damage and Glomerular Pressure;258
8.4.4.2;19.4.2 Kidney Damage and Autoregulation Loss;259
8.4.5;19.5 Conclusions;263
8.4.6;References;264
8.5;20 Disturbed Calcium–Phosphorus Metabolism/Arterial Calcifications: Consequences on Cardiovascular Function and Clinical Outcome;267
8.5.1;20.1 Introduction;267
8.5.2;20.2 Mechanisms of Arterial Calcification;268
8.5.3;20.3 Clinical Impact of Arterial Calcifications;270
8.5.4;20.4 Management and Prevention;271
8.5.5;20.5Conclusions;272
8.5.6;References;273
8.6;21 Role of Neurohormonal Activation in the Pathogenesis of Cardiovascular Complications in Chronic Kidney Disease;276
8.6.1;21.1 Introduction;276
8.6.2;21.2 Epidemiological Considerations;277
8.6.2.1;21.2.1 Increased Sympathetic Nervous System Activity;278
8.6.2.1.1;21.2.1.1 Renal Mechanisms of Increased Sympathetic Nervous System Activation;280
8.6.2.1.2;21.2.1.2 Neurogenic Hypertension in Kidney Disease;281
8.6.2.1.3;21.2.1.3 Reflex Increase in Sympathetic Nervous System Activity and Organ Damage;281
8.6.2.2;21.2.2 Renin–Angiotensin–Aldosterone System;283
8.6.2.3;21.2.3 Interactions Between the Sympathetic Nervous System and the Renin–Angiotensin System;285
8.6.3;References;285
8.7;22 Impaired Autonomic Blood Pressure and Blood Volume Control in Chronic Renal Failure;288
8.7.1;22.1 Introduction;288
8.7.2;22.2 Reflex Control of Circulation in Renal Failure;289
8.7.2.1;22.2.1 Arterial Baroreflex;289
8.7.2.2;22.2.2 Cardiopulmonary Reflex;291
8.7.2.3;22.2.3 Other Cardiovascular Reflexes;291
8.7.3;22.3 Mechanisms Responsible for Reflex Abnormalities;291
8.7.4;22.4 Consequences of Cardiovascular Reflex Dysfunction;292
8.7.5;22.5 Therapeutic Implications;293
8.7.6;References;293
8.8;23 Role of Novel Biomarkers in Chronic Kidney Disease: Urotensin II;295
8.8.1;23.1 Introduction;295
8.8.2;23.2 Notes on Urotensin II Biochemistry;296
8.8.3;23.3 Role of Urotensin II in the Cardiovascular System in Health and Disease;297
8.8.4;23.4 Role of Urotensin II in the Kidney and in Renal Diseases;298
8.8.5;23.5 Conclusions;301
8.8.6;References;302
8.9;24 Role of Novel Biomarkers in Chronic Kidney Disease: Renalase;305
8.9.1;24.1 Introduction;305
8.9.2;24.2 Renalase: Discovery and Characterization;306
8.9.3;24.3 Renalase Deficiency in Chronic Kidney Disease;307
8.9.4;24.4 Renalase Deficiency and hypertension;308
8.9.5;24.5 Renalase Deficiency and Myocardial Necrosis;309
8.9.6;24.6 Urinary Renalase and Acute Kidney Injury;309
8.9.7;24.7 Renalase Pathway;310
8.9.8;References;311
9;Section VI Regression/Progression of Chronic Kidney Disease;313
9.1;25 Diabetic Kidney Disease;314
9.1.1;25.1 Introduction;314
9.1.2;25.2 Physiopathology and Pathology;315
9.1.3;25.3 Factors Related to Diabetic Nephropathy Development and Progression;317
9.1.3.1;25.3.1 Hyperglycemia;318
9.1.3.2;25.3.2 Hypertension;318
9.1.3.3;25.3.3 Genetics;319
9.1.3.4;25.3.4 Proteinuria;320
9.1.3.5;25.3.5 Others;321
9.1.3.5.1;25.3.5.1 Smoking;321
9.1.3.5.2;25.3.5.2 Dyslipidemia;321
9.1.3.5.3;25.3.5.3 Diet;322
9.1.4;25.4 Prevention and Treatment;323
9.1.4.1;25.4.1 Screening for Urinary Albumin Excretion;324
9.1.4.1.1;25.4.1.1 GFR Estimation;324
9.1.4.1.2;25.4.1.2 Blood Pressure Measurement;324
9.1.4.2;25.4.2 Optimize Medical Management and Educate Patients;325
9.1.4.2.1;25.4.2.1 Glycemic Control;325
9.1.4.3;25.4.3 Blood Pressure Control and Renin–Angiotensin System Blockade;326
9.1.4.4;25.4.4 Studies in Normoalbuminuria Stage;326
9.1.4.5;25.4.5 Studies in Increased Urinary Albumin Excretion;328
9.1.4.6;25.4.6 Studies in Advanced DN;329
9.1.5;25.5 Discussion;330
9.1.6;References;331
9.2;26 Nondiabetic Kidney Disease;335
9.2.1;26.1 Introduction;336
9.2.2;26.2 Mechanisms of Progression of Chronic Nephropathies;337
9.2.2.1;26.2.1 Hypertension;337
9.2.2.2;26.2.2 Proteinuria;337
9.2.3;26.3 Renin–Angiotensin System Inhibitors as the First-step Therapy to Control Blood Pressure and Reduce Proteinuria;338
9.2.4;26.4 Is Dual RAS Blockade better than Single ACE Inhibitor/ARB Therapy?;339
9.2.5;26.5 Other Strategies to Further Decrease Proteinuria;342
9.2.5.1;26.5.1 Renin Inhibitors;342
9.2.5.2;26.5.2 Aldosterone Antagonists;343
9.2.5.3;26.5.3 Statins;343
9.2.5.4;26.5.4Vitamin D;344
9.2.5.5;26.5.5 Smoking Cessation;344
9.2.6;26.6 A Multimodal Strategy to Slow Progression of Chronic Proteinuric Nephropathies;345
9.2.7;26.7 Is Regression of Chronic Kidney Disease Possible?;346
9.2.8;26.8 Conclusions and Perspectives;347
9.2.9;References;347
10;Section VII Therapeutic Modalities;351
10.1;27 Approaches in the Management of Patients with Chronic Kidney Disease and Cardiovascular Disease;352
10.1.1;27.1 Introduction;352
10.1.2;27.2 Assessing Renal Function;353
10.1.3;27.3 Pathomechanisms;354
10.1.4;27.4 Interventions: The Dilemma of Incomplete Evidence;355
10.1.5;27.5 Preventive Strategies;355
10.1.5.1;27.5.1 Target Blood Pressure;355
10.1.5.1.1;27.5.1.1 Type of Antihypertensive Medication;357
10.1.6;27.6 Statins;359
10.1.7;27.7 Vitamin D and Phosphate–Calcium Metabolism;359
10.1.8;References;360
10.2;28 Trends in the Management of Cardiac Patients with Renal Functional Impairment;363
10.2.1;28.1 Introduction;363
10.2.1.1;28.1.1 Pharmacologic Therapeutic Strategies;364
10.2.1.1.1;28.1.1.1 Diuretics;364
10.2.1.1.2;28.1.1.2 Nonpharmacological Salt and Water Removal;366
10.2.1.1.3;28.1.1.3 Peritoneal Ultrafiltration;367
10.2.1.2;28.1.2 Extracorporeal Ultrafiltration: Equipment and Techniques;369
10.2.1.3;28.1.3 Extracorporeal Ultrafiltration: Recent Advances in Techniques;370
10.2.1.4;28.1.4 Ultrafiltration: Long-term Treatment;372
10.2.1.5;28.1.5 Effect of Ultrafiltration on HF Pathophysiology;372
10.2.1.6;28.1.6 Extracorporeal Ultrafiltration and Renal Function;373
10.2.1.7;28.1.7 Extracorporeal Ultrafiltration: Rate of Fluid Removal;374
10.2.1.8;28.1.8 Safety of Extracorporeal Therapies;375
10.2.1.8.1;28.1.8.1 Errors in Ultrafiltration;375
10.2.1.8.2;28.1.8.2 Air Embolism;375
10.2.1.8.3;28.1.8.3 Blood Leak;375
10.2.1.8.4;28.1.8.4 Bioincompatibility;376
10.2.1.8.5;28.1.8.5 Other Potential Complications;376
10.2.2;References;376
11;Subject Index;379