Cardiorenal Syndrome (eBook)
XV, 396 Seiten
Springer Italia (Verlag)
978-88-470-1463-3 (ISBN)
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.
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.
Preface 5
Table of Contents 6
List of Contributors 10
Section I Chronic Kidney Disease and Cardiovascular Disease Interrelationships 15
1 Links between Chronic Kidney Disease and Cardiovascular Disease: A Bidirectional Relationship 16
1.1 Introduction 16
1.2 Definition 17
1.3 Chronic Kidney Disease as a Promoter of Cardiovascular Disease 17
1.3.1 Epidemiology 17
1.3.2 Pathophysiologic Mechanisms 18
1.3.2.1 Atherosclerosis 19
1.3.2.2 Arteriosclerosis 20
1.3.2.3 Endothelial Dysfunction 21
1.3.2.4 Uremia-Related CVD 22
1.3.3 Course of CVD in CKD 22
1.4 CVD in Kidney Transplant Recipients 22
1.5 Cardiac Disease as a Promoter of Kidney Dysfunction 23
1.6 Conclusions 24
References 25
2 Cardiorenal versus Renocardiac Syndrome 28
2.1 Introduction 28
2.2 Heart Failure as a Cause of Kidney Failure (Cardiorenal Syndrome) 29
2.2.1 Ventricular Dilation in Congestive Heart Failure 29
2.2.2 Left Ventricular Mass Index and Congestive Heart Failure 31
2.2.3 Blunted Atrial–Renal Reflexes and Chronic Heart Failure 31
2.2.4 Neurohormones and Chronic Heart Failure 31
2.2.4.1 Renin–Angiotensin–Aldosterone System 31
2.2.4.2 Sympathetic Nervous System 33
2.2.4.3 Arginine Vasopressin 33
2.2.5 Cardiorenal Intersection in Heart Failure 34
2.3 Chronic Kidney Disease as a Pathogenic Factor for Cardiovascular Disease (Renocardiac Syndrome) 36
2.3.1 Accelerated Atherosclerosis in Chronic Kidney Disease 36
2.3.2 Role of Traditional Risk Factors and Cardiovascular Outcomes in Patients with Chronic Kidney Disease 37
2.3.2.1 Hypertension 37
2.3.2.2 Diabetes Mellitus 38
2.3.2.3 Dyslipidemia 39
2.3.3Novel Risk Factors in Cardiovascular Disease Progression in Patients with ChronicKidney Disease 40
2.3.3.1 Anemia 40
2.3.3.2 Oxidative Stress 41
2.3.3.3 Endothelial Dysfunction 41
2.3.3.4 Lipoprotein (a) 41
2.3.3.5 Hyperhomocysteinemia 42
2.3.3.6Inflammation and High-Sensitivity C-Reactive Protein 42
2.3.3.7 Accelerated Coronary Calcification 43
2.3.3.8 Other Novel Risk Factors 43
2.4 Chronic Kidney Disease and Valvular Heart Disease 43
2.5 Chronic Kidney Disease and Arrhythmias 44
2.6 Conclusions 44
References 45
Section IICrosstalk between the CardiovascularSystem and the Kidney 48
3 Non-Pressure-Related DeleteriousEffects of Excessive Dietary Sodium 49
3.1 Introduction 49
3.2 Measurement of 24-Hour Urinary Sodium is the Gold Standard for Estimating Sodium Intake 50
3.3 Influence of Sodium Intake on Subclinical Organ Damage 50
3.4 Does the Influence of Dietary Sodium on Target-Organ Damage Translate into a Difference in Risk? 52
3.5 Studies on the Effect of Salt Restriction 52
3.6 Is Reduction in Dietary Sodium Associated with a Reduction in Cardiovascular Risk? 53
3.7 Evidences in Favor of a Direct Effect of Dietary Sodium 53
3.8 Mechanism(s) Involved in the Deleterious Effect of Salt 54
3.9 Conclusions 56
References 57
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
4.1 Renin–Angiotensin System in Vascular and Renal Diseases: From the Classic View to the New and Complex System 61
4.2 Pharmacological Blockade of Renin–Angiotensin System in Vascular and Renal Diseases 63
4.3 Common Responses to Angiotensin II in Vascular and Renal Diseases: Modulation of Fibrosis and Inflammation 64
4.3.1 Angiotensin II and Cell Growth Regulation in Vascular and Renal Diseases 65
4.3.2 AngII Regulates Fibrosis via AT1 receptor: Role of CTGF and Smad Signaling Pathway 65
4.3.3 Role of Angiotensin II in the Inflammatory Response in Vascular and Renal Diseases 67
4.3.4 Active Role of AngII in Different Steps of Atherosclerosis 70
4.4 Role of Angiotensin Peptides in Vascular and Renal Diseases 70
4.4.1 AngIV in Cardiovascular Damage 71
4.4.2 Ang-(1–7) in Renal and Cardiovascular Damage 71
4.4.3 Conclusions 72
References 73
Section III Chronic Kidney Disease as a Risk forCardiovascular Disease 75
5 Cardiorenal Continuum 76
5.1 Introduction 76
5.2 Cardiovascular Disease Associated with Renal Disease: Evidences Along the Continuum 78
5.2.1 Global Therapeutic Approach Focused on Renal Outcomes 84
References 85
6 Definition and Classification of Stages of Chronic Kidney Disease: Screening for Chronic Kidney Disease 89
6.1 Introduction 89
6.2 Definition of Chronic Kidney Disease 90
6.3 Classification of Chronic Kidney Disease 90
6.4 Chronic Kidney Disease Screening 92
6.5 Conclusions 96
References 96
7 Cardiovascular Disease Risk Factors in Chronic Kidney Disease: Traditional, Nontraditional, and Uremia-related Threats 98
7.1 Introduction 98
7.2 Epidemiological Considerations 99
7.2.1 Difficulties in Describing Causes of Death 99
7.2.2 Effects of Changing Demographics and Race on CVD in CKD 100
7.2.3 Reverse Epidemiology 100
7.3 Traditional Risk Factors 101
7.3.1 Age, Gender, and Smoking 101
7.3.2 Diabetes Mellitus 101
7.3.3Hypertension 102
7.3.4 Insulin Resistance 102
7.3.5 Dyslipidemia 102
7.4 Nontraditional and/or Uremia-specific Risk Factors 103
7.4.1 Renal Failure Per Se 103
7.4.2 Oxidative Stress 103
7.4.3 Hyperhomocysteinemia 104
7.4.4 Inflammation 105
7.4.5 Endothelial dysfunction 106
7.4.6 Secondary Hyperparathyroidism and Mineral Metabolism 107
7.4.7 Cardiovascular Calcification 107
7.4.8 Autonomic Dysfunction 108
7.4.9 Anemia 108
7.4.10 Hormonal Derangements 108
References 109
8 Increased Levels of Urinary Albumin: A Cardiovascular Risk Factor and a Target for Treatment 112
8.1Introduction 112
8.2 Definition of Albuminuria 113
8.2.1 How Do We Measure Albuminuria? 113
8.2.1.1 Protein or Albumin? 113
8.2.1.2 Measurement Technique 114
8.2.1.3 Urine Collection 114
8.2.1.4 Fresh or Frozen Sample? 116
8.3 Epidemiology 116
8.4 Pathophysiology 117
8.5 CVD Risk Prediction 117
8.6 Targeting Albuminuria for CVD Risk Protection 119
References 121
9 Microalbuminuria and Kidney Disease: An Evidence-based Perspective 124
9.1 Introduction 124
9.2 Definition of Microalbuminuria 125
9.3 Prevalence of Microalbuminuria 126
9.4 Pathophysiology of Microalbuminuria 126
9.5 Cardiovascular Risk 127
9.5.1 Hypertension 127
9.5.2 Hyperinsulinemia 128
9.5.3 Endothelial Dysfunction 128
9.5.4 Dyslipidemia 129
9.5.5 C-reactive Protein 130
9.5.6 Genetic Associations 130
9.5.7 Vascular Risk Assessment 130
9.6 Prognostic Implications 130
9.7 Chronic Kidney Disease 132
9.8 Therapeutic Intervention and Cardiorenal Disease Risk Reduction 133
9.9 Conclusions 134
References 135
10 Cardiometabolic Syndrome 138
10.1 Introduction 138
10.2 Definition and Origins of Cardiometabolic Syndrome 139
10.3 Cardiometabolic Syndrome and CKD Risk 141
10.3.1 Microalbuminuria 141
10.3.2 CKD 141
10.4 Proposed Mechanisms of CKD Risk in Cardiometabolic Syndrome 143
10.4.1 Pathologic Findings 144
10.4.2 Lipotoxicity 144
10.4.3 Inflammation 144
10.4.4 Activation of the Renin–Angiotensin System (RAS) Axis 145
10.4.5 Obesity and Obesity-Related Hemodynamic Factors 145
10.4.6 Hyperuricemia 145
10.5Cardiometabolic Syndrome and CVD Risk 146
10.5.1 Studies in the General Population 146
10.5.2 Studies in CKD Populations 146
10.6 Implications for CKD and CVD Risk Prediction and Risk Reduction 147
10.6.1 Risk Prediction 147
10.6.2 Risk Reduction Strategies 148
References 149
11 Diabetes Mellitus: Is the Presence of Nephropathy Important as a Cardiovascular Risk Factor for Cardiorenal Syndrome? 152
11.1 Introduction 153
11.2 Diabetes Mellitus 153
11.2.1 Diabetes and the Kidney 153
11.2.2 Diabetes and the Heart 154
11.2.3 Micro- and Macroalbuminuria in Diabetes and CVD Risk 154
11.3 CKD and CVD 155
11.4 Pathogenesis 158
11.5 Treatment 159
11.6 Conclusions 160
Reference 161
Section IV Spectrum of Cardiovascular Disease in Chronic Kidney Disease 165
12 Cardiovascular Disease: Coronary Artery Disease and Coronary Artery Calcification 166
12.1 Introduction 166
12.2 Coronary Artery Disease in Chronic Kidney Disease 167
12.2.1 Etiology and Pathogenesis of CAD in CKD 167
12.2.2 Potential Mechanisms of Accelerated Atherosclerosis in CKD 168
12.2.2.1 Visceral Adiposity and Atherosclerosis in CKD 168
12.2.2.2 Serum Vitamin D, Fibroblast Growth Factor-23 and Alkaline Phosphatase 169
12.2.2.3 Hypertension 170
12.2.2.4 Dyslipidemia 170
12.2.2.5 Inflammation and Oxidative Stress 170
12.2.3 Clinical Presentation and Diagnosis of CAD in CKD 171
12.2.3.1 Laboratory Diagnosis of Acute Coronary Syndromes 171
12.2.3.2 Stress Tests for Diagnosis of Chronic Myocardial Ischemia 171
12.2.3.3 Electron Beam Computed Tomography 171
12.3 Therapy for CAD in CKD 172
12.3.1 Antiplatelet Agents 172
12.3.2 Beta Blockers 172
12.3.3Angiotensinogen-converting Enzyme (ACE) Inhibitors/AngiotensinReceptor Blockers (ARB) 173
12.3.4 Lipid-Lowering Therapy 173
12.4 Coronary Revascularization in CKD 174
12.5 Coronary Calcification in CKD 175
References 176
13 Cardiomyopathy in Chronic Kidney Disease and in End-stage Renal Disease 179
13.1 Introduction 180
13.2 Left Ventricular Mass and Function in Stages 3–5 Chronic Kidney Disease Patients and Dialysis Patients 180
13.2.1 Problem of Appropriate Indexing 180
13.2.2 Cardiomyopathy in Stages 3–5 Chronic Kidney Disease Patients 181
13.2.3 Cardiomyopathy in End-stage Renal Disease Patients 183
13.3 Drug Treatment of Left-Ventricular Disorders in Chronic Kidney Disease and End-stage Renal Disease Patients 186
13.4 Dialysis Treatment Modalities, Implantable Cardioverters, and Cardiac Resynchronization in End-stage Renal Disease Patients with Left-ventricular Systolic Dysfunction 187
13.5Conclusions 188
References 189
14 Pathophysiological Mechanisms and Prognostic Significance of Renal Functional Impairment in Cardiac Patients 192
14.1 Definition of Cardiorenal Syndrome 193
14.2 Prevalence of Renal Functional Impairment in HF 193
14.3 Pathophysiological Mechanisms 194
14.3.1 Complex Mechanisms Involved in ECFV (Dys)regulation in HF 195
14.3.2 CRC: Mechanisms Beyond ECFV Regulation 196
14.3.2.1 RAAS 197
14.3.2.2 Balance Between NO and ROS 197
14.3.2.3 Inflammation 197
14.3.2.4 SNS 197
14.3.3 Importance of Central Venous Pressure 198
14.3.4 Anemia: The Third Condition of a Deadly Triad? 199
14.4 Prognostic Significance 200
14.4.1 Chronic HF 200
14.4.2 Acute HF 201
References 203
15 Stroke 207
15.1 Introduction 207
15.2 Epidemiology 208
15.2.1 Gauging Stroke Risk in CKD 208
15.3 Mechanisms of Stroke Occurrence in CKD 208
15.3.1 Blood Pressure 208
15.3.2 Dyslipidemia 209
15.3.3 Anemia 209
15.3.4 Proteinuria 209
15.4 Management of Stroke Risk in CKD 211
15.4.1 Hypertension 211
15.4.2 Dyslipidemia 213
15.4.3 Anemia 214
15.4.4 Other Targets 214
15.5 Conclusions 215
References 215
Section V Mechanisms of Cardiovascular Complications 218
16 Uremic Toxins 219
16.1 Introduction 219
16.2 Cardiovascular Implications 220
16.3 Classification of Uremic Retention Solutes 220
16.3.1 Advanced Glycation End Products 222
16.3.2 Advanced Oxidation Protein Products 223
16.3.3 Angiogenin – Degranulation-inhibiting Protein I 223
16.3.4 Angiotensin II Variants 224
16.3.5 Complement Factor D 224
16.3.6 p-Cresyl Sulphate 224
16.3.7 Cytokines 225
16.3.8 Dinucleoside Polyphosphates 225
16.3.9 Guanidines 226
16.3.10 Homocysteine 226
16.3.11 Immunoglobulin Light Chains 227
16.3.12 Indoxyl Sulphate 227
16.3.13 Leptin 228
16.3.14 B2 Microglobulin and AGE-modified B2 Microglobulin 228
16.3.15 Oxalic Acid 229
16.3.16 Phenylacetic Acid 229
16.4 Conclusions 230
References 231
17 Endothelial Dysfunction, Nitric OxideBioavailability, and AsymmetricDimethyl Arginine 235
17.1 Introduction 235
17.2 Basic Biochemistry of the NO System 236
17.3 Endothelial Dysfunction: Molecular Mechanisms 237
17.4 Endothelial NOS Activity Modulation and Factors Affecting NO Bioavailability 237
17.5 Biomarkers of Endothelial Function 239
17.6 Endothelial and Renal Dysfunction in Essential Hypertension and in the Aging Kidney 240
17.7 Endogenous Inhibitors of the Nitric Oxide System, CKD, and Cardiorenal Risk 242
17.8 ADMA as a Risk Factor for CKD 242
References 243
18 Pathophysiologic Link between Atherosclerosis and Nephrosclerosis 245
18.1 Introduction 245
18.2 Lipid Accumulation 246
18.3 Inflammation 247
18.4 Cellular Proliferation 249
18.5Extracellular Matrix Turnover 249
18.6 Thrombosis 251
References 252
19 Aortic Stiffness, Kidney Disease, and Renal Transplantation 254
19.1 Introduction 254
19.2 Large Artery Damage in Chronic Renal Disease 255
19.2.1 Individuals with ESRD 255
19.2.2 Individuals with Mild to Moderate Renal Insufficiency 256
19.3 Calcium and Arterial Calcifications 257
19.4 Pulse Pressure, Renal Autoregulation, and End-organ Damage 258
19.4.1 Kidney Damage and Glomerular Pressure 258
19.4.2 Kidney Damage and Autoregulation Loss 259
19.5 Conclusions 263
References 264
20 Disturbed Calcium–Phosphorus Metabolism/Arterial Calcifications: Consequences on Cardiovascular Function and Clinical Outcome 267
20.1 Introduction 267
20.2 Mechanisms of Arterial Calcification 268
20.3 Clinical Impact of Arterial Calcifications 270
20.4 Management and Prevention 271
20.5Conclusions 272
References 273
21 Role of Neurohormonal Activation in the Pathogenesis of Cardiovascular Complications in Chronic Kidney Disease 276
21.1 Introduction 276
21.2 Epidemiological Considerations 277
21.2.1 Increased Sympathetic Nervous System Activity 278
21.2.1.1 Renal Mechanisms of Increased Sympathetic Nervous System Activation 280
21.2.1.2 Neurogenic Hypertension in Kidney Disease 281
21.2.1.3 Reflex Increase in Sympathetic Nervous System Activity and Organ Damage 281
21.2.2 Renin–Angiotensin–Aldosterone System 283
21.2.3 Interactions Between the Sympathetic Nervous System and the Renin–Angiotensin System 285
References 285
22 Impaired Autonomic Blood Pressure and Blood Volume Control in Chronic Renal Failure 288
22.1 Introduction 288
22.2 Reflex Control of Circulation in Renal Failure 289
22.2.1 Arterial Baroreflex 289
22.2.2 Cardiopulmonary Reflex 291
22.2.3 Other Cardiovascular Reflexes 291
22.3 Mechanisms Responsible for Reflex Abnormalities 291
22.4 Consequences of Cardiovascular Reflex Dysfunction 292
22.5 Therapeutic Implications 293
References 293
23 Role of Novel Biomarkers in Chronic Kidney Disease: Urotensin II 295
23.1 Introduction 295
23.2 Notes on Urotensin II Biochemistry 296
23.3 Role of Urotensin II in the Cardiovascular System in Health and Disease 297
23.4 Role of Urotensin II in the Kidney and in Renal Diseases 298
23.5 Conclusions 301
References 302
24 Role of Novel Biomarkers in Chronic Kidney Disease: Renalase 305
24.1 Introduction 305
24.2 Renalase: Discovery and Characterization 306
24.3 Renalase Deficiency in Chronic Kidney Disease 307
24.4 Renalase Deficiency and hypertension 308
24.5 Renalase Deficiency and Myocardial Necrosis 309
24.6 Urinary Renalase and Acute Kidney Injury 309
24.7 Renalase Pathway 310
References 311
Section VI Regression/Progression of Chronic Kidney Disease 313
25 Diabetic Kidney Disease 314
25.1 Introduction 314
25.2 Physiopathology and Pathology 315
25.3 Factors Related to Diabetic Nephropathy Development and Progression 317
25.3.1 Hyperglycemia 318
25.3.2 Hypertension 318
25.3.3 Genetics 319
25.3.4 Proteinuria 320
25.3.5 Others 321
25.3.5.1 Smoking 321
25.3.5.2 Dyslipidemia 321
25.3.5.3 Diet 322
25.4 Prevention and Treatment 323
25.4.1 Screening for Urinary Albumin Excretion 324
25.4.1.1 GFR Estimation 324
25.4.1.2 Blood Pressure Measurement 324
25.4.2 Optimize Medical Management and Educate Patients 325
25.4.2.1 Glycemic Control 325
25.4.3 Blood Pressure Control and Renin–Angiotensin System Blockade 326
25.4.4 Studies in Normoalbuminuria Stage 326
25.4.5 Studies in Increased Urinary Albumin Excretion 328
25.4.6 Studies in Advanced DN 329
25.5 Discussion 330
References 331
26 Nondiabetic Kidney Disease 335
26.1 Introduction 336
26.2 Mechanisms of Progression of Chronic Nephropathies 337
26.2.1 Hypertension 337
26.2.2 Proteinuria 337
26.3 Renin–Angiotensin System Inhibitors as the First-step Therapy to Control Blood Pressure and Reduce Proteinuria 338
26.4 Is Dual RAS Blockade better than Single ACE Inhibitor/ARB Therapy? 339
26.5 Other Strategies to Further Decrease Proteinuria 342
26.5.1 Renin Inhibitors 342
26.5.2 Aldosterone Antagonists 343
26.5.3 Statins 343
26.5.4Vitamin D 344
26.5.5 Smoking Cessation 344
26.6 A Multimodal Strategy to Slow Progression of Chronic Proteinuric Nephropathies 345
26.7 Is Regression of Chronic Kidney Disease Possible? 346
26.8 Conclusions and Perspectives 347
References 347
Section VII Therapeutic Modalities 351
27 Approaches in the Management of Patients with Chronic Kidney Disease and Cardiovascular Disease 352
27.1 Introduction 352
27.2 Assessing Renal Function 353
27.3 Pathomechanisms 354
27.4 Interventions: The Dilemma of Incomplete Evidence 355
27.5 Preventive Strategies 355
27.5.1 Target Blood Pressure 355
27.5.1.1 Type of Antihypertensive Medication 357
27.6 Statins 359
27.7 Vitamin D and Phosphate–Calcium Metabolism 359
References 360
28 Trends in the Management of Cardiac Patients with Renal Functional Impairment 363
28.1 Introduction 363
28.1.1 Pharmacologic Therapeutic Strategies 364
28.1.1.1 Diuretics 364
28.1.1.2 Nonpharmacological Salt and Water Removal 366
28.1.1.3 Peritoneal Ultrafiltration 367
28.1.2 Extracorporeal Ultrafiltration: Equipment and Techniques 369
28.1.3 Extracorporeal Ultrafiltration: Recent Advances in Techniques 370
28.1.4 Ultrafiltration: Long-term Treatment 372
28.1.5 Effect of Ultrafiltration on HF Pathophysiology 372
28.1.6 Extracorporeal Ultrafiltration and Renal Function 373
28.1.7 Extracorporeal Ultrafiltration: Rate of Fluid Removal 374
28.1.8 Safety of Extracorporeal Therapies 375
28.1.8.1 Errors in Ultrafiltration 375
28.1.8.2 Air Embolism 375
28.1.8.3 Blood Leak 375
28.1.8.4 Bioincompatibility 376
28.1.8.5 Other Potential Complications 376
References 376
Subject Index 379
| Erscheint lt. Verlag | 4.10.2010 |
|---|---|
| Zusatzinfo | XV, 396 p. |
| Verlagsort | Milano |
| Sprache | englisch |
| Themenwelt | Medizinische Fachgebiete ► Innere Medizin ► Kardiologie / Angiologie |
| Medizinische Fachgebiete ► Innere Medizin ► Nephrologie | |
| Schlagworte | cardiorenal syndorme • Cardiovascular • Cardiovascular Disease • Chronic Kidney Disease • Hypertension • Inflammatory Markers • related cv risk factors • uremia |
| ISBN-10 | 88-470-1463-8 / 8847014638 |
| ISBN-13 | 978-88-470-1463-3 / 9788847014633 |
| Haben Sie eine Frage zum Produkt? |
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