Urinary Tract Stone Disease (eBook)

Mr Nagaraja Rao is currently a Consultant Urological Surgeon at South Manchester University Hospital, an Honorary Consultant Urological Surgeon at Royal Manchester Children's Hospital, and a Consultant Urological Surgeon at BUPA Hospital, Manchester. He is also a President of the Eurolithiasis Society and a Member of Section Office at the European Association of Urology. Dr John Kavanagh is Principal Research Biochemist at the University of Manchester, UK and is well known in the field of urinary stones. Dr Glenn M. Preminger is Professor of Urologic Surgery at the Division of Urologic Surgery, Duke University Medical Center, Durham, NC, USA. He specializes in the medical and surgical management of kidney stone disease and the use of shock wave lithotripsy, and minimally invasive treatment of benign prostatic hyperplasia (enlarged prostate). He has conducted research in various aspects of urology, including minimally invasive treatments for urologic diseases, urinary tract obstructions, enlarged prostate, and renal and ureteral stones.

Urinary Tract StoneDisease 3
Preface 5
Contents 7
Contributors 13
Part I Basic Sciences 21
1: Epidemiology 22
1.1 Introduction 22
1.2 Prevalence 22
1.3 Incidence 23
1.4 Recurrence Rates 23
1.5 Risk Factors 23
1.5.1 Non-dietary 23
1.5.1.1 Family History 23
1.5.1.2 Race/Ethnicity 23
1.5.1.3 Systemic Disorders 23
1.5.1.4 Environmental Factors 24
1.5.2 Dietary Factors 24
1.5.2.1 Calcium 24
1.5.2.2 Oxalate 24
1.5.2.3 Other Nutrients 25
1.5.2.4 Fluid Intake and Beverages 25
1.6 Urinary Factors 25
1.7 Conclusions 26
References 26
2: Genetics and Molecular Biology of Renal Stones 28
2.1 Introduction 28
2.2 Genetic Linkage Studies 28
2.3 Genetic Association Studies 29
2.4 Animal Models of Genetic Disease 31
2.5 Future Areas of Study 32
2.6 Conclusions 32
References 33
3: Physicochemical Aspects of Uro-crystallization and Stone Formation 35
3.1 Introduction 36
3.2 Supersaturation 36
3.2.1 Different States of Saturation 36
3.2.2 Supersaturation Equations 37
3.2.3 Estimating Urinary Supersaturation 38
3.2.4 Solubility 38
3.3 Classical Crystallization Processes 39
3.3.1 Nucleation 39
3.3.1.1 Homogeneous Nucleation 40
3.3.1.2 Heterogeneous Nucleation 41
3.3.1.3 The Metastable Limit and Induction Time 42
3.3.2 Crystal Growth 43
3.3.2.1 Desaturation Profile 43
3.3.2.2 Stoichiometry 43
3.3.3 Aggregation 44
3.4 Nonclassical Crystallization 45
3.5 Other Crystallization Processes 46
3.5.1 Promotion/Inhibition 46
3.5.2 Morphology/Aging 46
3.6 Conclusions 46
References 47
4: The Possible Roles of Inhibitors, Promoters, and Macromolecules in the Formation of Calcium Kidney Stones 49
4.1 Introduction 49
4.2 Calcium Oxalate Crystallization in the Urinary Tract 50
4.2.1 Free-Particle Stone Formation 50
4.2.2 Fixed-Particle Stone Formation 51
4.2.3 The Inhibitor Theory of Stone Formation 51
4.3 Measuring Inhibition and Promotion of Crystallization and Cell Adhesion 52
4.3.1 The Complexity of Crystallization 52
4.3.1.1 Uncertainty About Working Material: Identity, Purity, and Source 52
4.3.1.2 A Multiplicity of Methodologies 52
4.3.1.3 Necessary but Imperfect: Experimental Cell Models 53
4.3.1.4 What You See Is What You Get: Not Necessarily What Actually Happens in Real Life 53
4.4 Inhibitors and Promoters of CaOx Crystallization 53
4.4.1 Promoters of CaOx Crystal Nucleation 53
4.4.2 Inhibitors of CaOx Crystallization 54
4.4.2.1 The Effect of Urine on CaOx Crystallization 54
4.5 Inhibitors and Promoters of CaOx Crystal–Cell Adhesion 54
4.5.1 Urine and Generic Urinary Macromolecules 54
4.5.2 Macromolecular Inhibitors of Cell Adhesion 55
4.5.3 Macromolecular Promoters of Crystal–Cell Adhesion 55
4.5.4 A Fortunate Adversity: Phagocytosis, Intracrystalline Proteins, and Crystal Dissolution 55
4.5.4.1 Intracrystalline Proteins 55
Summary 56
4.6 Low Molecular Weight Inhibitors 56
4.6.1 Pyrophosphate 56
4.6.1.1 Effect of Pyrophosphate on Crystallization 56
4.6.1.2 Urinary Excretion of Pyrophosphate 57
4.6.1.3 Summary 57
4.6.2 Magnesium 57
4.6.2.1 Effect of Magnesium on Crystallization 57
4.6.2.2 Urinary Excretion of Magnesium 57
4.6.2.3 Effect of Magnesium in Experimental Models 57
4.6.2.4 Summary 57
4.6.3 Citrate 58
4.6.3.1 Effect of Citrate on Crystallization 58
4.6.3.2 Urinary Excretion of Citrate and Effects in Experimental Models 58
4.6.3.3 Summary 58
4.6.4 Phytic Acid (Inositol 1,2,3,4,5,6-Hexakisphosphate) 58
4.6.4.1 Summary 59
4.6.5 Summary: Low Molecular Weight Inhibitors 59
4.7 Macromolecular Promoters and Inhibitors 59
4.7.1 Glycosaminoglycans (GAGs) 59
4.7.1.1 GAGs in Kidney Stones 59
4.7.1.2 Chondroitin Sulfate (CS) 59
4.7.1.3 Heparan Sulfate (HS) 59
4.7.1.4 Hyaluronic Acid (HA) 60
4.7.1.5 Heparin 60
4.7.1.6 Synthetic GAGs 60
4.7.1.7 Urinary Excretion of GAGs 60
4.7.1.8 Summary: Are Urinary GAGs Important in Stone Formation? 60
4.8 Proteins 61
4.8.1 Proteins in Kidney Stones 61
4.8.2 Tamm–Horsfall Glycoprotein (THG) 62
4.8.2.1 Effect of THG on Crystallization 62
4.8.2.2 Effect of THG on Crystal–Cell Interaction 63
4.8.2.3 Structural Features of THG 63
4.8.2.4 Expression of THG in Animal and Cell Models 63
4.8.2.5 Urinary Excretion of THG 63
4.8.2.6 Summary 63
4.8.3 Osteopontin 63
4.8.3.1 Effect of OPN on Crystallization 64
4.8.3.2 Effect of OPN on Crystal–Cell Interaction 64
4.8.3.3 Expression of OPN in Animal and Cell Models 64
4.8.3.4 Urinary Excretion of OPN 64
4.8.3.5 Summary 65
4.8.4 Prothrombin Fragment 1 (PTF1) 65
4.8.4.1 Effect of PTF1 on Crystallization 65
4.8.4.2 Effect of PTF1 on Crystal–Cell Interaction 65
4.8.4.3 Expression of PTF1 in Animal and Cell Models 65
4.8.4.4 Urinary Excretion of PTF1 66
4.8.4.5 Summary 66
4.8.5 Inter-a-Inhibitor (IaI) 66
4.8.5.1 Effect of IaI on Crystallization 66
4.8.5.2 Effect of IaI on Crystal–Cell Interaction 66
4.8.5.3 Expression of IaI in Animal and Cell Models 66
4.8.5.4 Urinary Excretion of IaI 67
4.8.5.5 Summary 67
4.8.6 Calgranulin (Calprotectin) 67
4.8.7 Human Serum Albumin (HSA) 67
4.8.7.1 Summary 67
4.8.8 Fibronectin 68
4.9 Conclusions 68
References 69
5: Renal Cellular Dysfunction/Damage and the Formation of Kidney Stones 79
5.1 Introduction 79
5.2 Supersaturation and Crystallization of Calcium Oxalate 80
5.3 Intrinsic Factors: Genetic Basis of Cellular Dysfunction 80
5.3.1 Calciuria 80
5.3.2 Oxaluria 83
5.3.3 Citraturia 84
5.3.4 Pyrophosphaturia 84
5.3.5 Macromoleculuria 84
5.4 Extrinsic Factors: Renal Injury and Cellular Dysfunction 86
5.4.1 Clinical Studies 86
5.4.2 Animal Model Studies 87
5.4.3 Renal Cell Injury and Crystal Nucleation 88
5.4.4 Renal Cell Injury and Crystal Retention 88
5.4.4.1 Crystal Formation in the Interstitium 89
5.4.4.2 Crystal Attachment to Renal Epithelium 89
5.4.4.3 Crystals Not Travelling with the Urinary Flow 91
5.4.4.4 Crystal Aggregation 91
5.4.5 Renal Cell Injury, Crystallization Modulators, Inflammation, and Fibrosis 91
5.4.5.1 Animal Model Studies 91
5.4.5.2 Tissue Culture Studies 92
5.4.6 Shock Wave Lithotripsy and Cellular Dysfunction 93
5.5 Signaling Pathways 93
5.6 Formation of Stone Nidus and Development of Stone 95
5.7 Conclusions 96
References 98
6: Interaction of Stone Components with Cells and Tissues 105
6.1 Introduction 105
6.2 Sites of Crystal Attachment 105
6.2.1 Interstitial Calcification and Randall’s Plaques 106
6.2.2 Surface Adherence or Nucleation of Crystals 106
6.3 Consequences of Crystal Adherence 107
6.3.1 Crystal Internalization 108
6.3.2 Dissolution of Crystals and Transcytosis 109
6.4 Cellular Consequences of Crystal–Cell Interaction 109
6.5 Crystal Adherence Specificity 110
6.5.1 Features Responsible for Specificity 110
6.5.2 Molecules Responsible for Crystal Adherence 112
6.5.3 Functional Group Requirements for Crystal–Cell Adherence 113
6.6 Uric Acid Attachment Sites 114
6.7 Brushite and Apatite Attachment Sites 114
6.8 Cell or Tissue Damage as a Prerequisite to Stone Formation 114
6.8.1 Hyperoxaluria 114
6.8.2 Hypercalciuria 115
6.8.3 Hyperphosphaturia 116
6.8.4 Hyperuricosuria 116
6.9 Conclusions 116
References 117
7: Randall’s Plaques 120
7.1 Historical Perspective 120
7.2 Prevalence of Randall’s Plaques and Umbilicated Calculi 121
7.3 Origin of Randall’s Plaques 123
7.4 Mechanism of Plaque-Associated Stone Formation 124
7.5 Risk Factors for Randall’s Plaque Formation 126
7.6 Implications for Clinical Practice 128
7.7 Conclusions 128
References 128
8: Dietary Factors 130
8.1 Introduction 130
8.2 Fluid Intake 130
8.2.1 Citrus Juices 131
8.2.2 Other Fruit Juices 131
8.2.3 Coffee and Tea 132
8.2.4 Soft Drinks 132
8.2.5 Alcoholic Beverages 132
8.2.6 Water 133
8.3 Protein 133
8.4 Carbohydrates 134
8.5 Fat 135
8.6 Oxalate 135
8.7 Calcium 136
8.8 Magnesium 136
8.9 Sodium 136
8.10 Ascorbic Acid 136
8.11 Phytate 137
8.12 Purines 137
8.13 Dietary Habits 137
8.14 Conclusions 138
References 138
9: Obesity, Metabolic Syndrome, and Stones 142
9.1 Introduction 142
9.2 Obesity, Metabolic Syndrome, Low Urine pH, and Uric Acid Stone Formation 143
9.2.1 Pathophysiology 143
9.2.2 Uric Acid Stones, Metabolic Syndrome, and Insulin Resistance 143
9.3 Bariatric Surgery and Calcium Oxalate Stone Formation 144
9.3.1 Epidemiologic Background 144
9.3.2 Renal Complications of Bariatric Surgery 144
9.3.3 Pathogenesis of Hyperoxaluria After Bariatric Surgery 145
9.4 Conclusions 145
References 145
10: Stone Disease in Animals 147
10.1 Introduction 147
10.2 Epidemiology 147
10.3 Clinical Signs 150
10.4 Dog and Cat Urine Composition 151
10.5 Canine Uroliths 151
10.5.1 Struvite 152
10.5.1.1 Epidemiology 152
10.5.1.2 Pathophysiology 152
10.5.1.3 Treatment and Prevention 153
10.5.2 CaOx 154
10.5.2.1 Epidemiology 154
10.5.2.2 Pathophysiology 154
10.5.2.3 Treatment and Prevention 154
10.5.3 Purine 155
10.5.3.1 Epidemiology 155
10.5.3.2 Pathophysiology 155
10.5.3.3 Treatment and Prevention 156
10.5.4 Cystine 156
10.5.4.1 Pathophysiology 156
10.5.4.2 Treatment and Prevention 157
10.5.5 Silica 157
10.5.6 Calcium Phosphate 157
10.5.7 Pyrophosphate and DSBC 158
10.5.8 Compound Uroliths 158
10.5.9 Drug Metabolites Appearing as Urinary Stones 158
10.6 Feline Uroliths 158
10.6.1 Struvite 158
10.6.1.1 Epidemiology 158
10.6.1.2 Pathophysiology 158
10.6.1.3 Urinary Plugs 159
10.6.1.4 Treatment and Prevention 159
10.6.2 CaOx 160
10.6.2.1 Epidemiology 160
10.6.2.2 Pathophysiology 160
10.6.2.3 Treatment and Prevention 160
10.6.3 Purine 161
10.6.3.1 Epidemiology 161
10.6.3.2 Pathophysiology 162
10.6.3.3 Treatment and Prevention 162
10.6.4 Calcium Phosphate 162
10.6.5 Cystine 162
10.6.6 Potassium Magnesium Pyrophosphate 162
10.6.7 DSBC 162
10.6.8 Compound Uroliths and Drug Metabolite Containing Uroliths 163
10.7 Conclusions 163
References 163
11: Pathogenesis of Stones: Summary of Current Concepts 167
11.1 Introduction 167
11.2 Idiopathic Hypercalciura 168
11.3 Hyperparathyroidism 168
11.4 Hyperoxaluria 168
11.5 Hypocitraturia 168
11.6 Hyperuricosuria 168
11.7 Physicochemical Factors, Inhibitors, and Promoters 168
11.8 Oxalate Degrading Bacteria 169
11.9 Randall’s Plaque 169
11.10 Genetics 170
11.10.1 Hypercalciuria 170
11.10.2 Hyperoxaluria 170
11.10.3 Hypocitraturia 170
11.10.4 Hyperurocosuria 170
11.10.5 Cystinuria 170
11.10.6 Experts’ Comments 170
11.11 Conclusions 171
References 171
Part II Basic Sciences 173
12: Calcium Metabolism and Hypercalciuria 174
12.1 Calcium Metabolism 174
12.2 Calcium Transport in the Nephron 174
12.3 Hormonal Effects on Calcium Reabsorption 175
12.3.1 PTH Effects on the Kidney 175
12.3.2 Role of Vitamin D 176
12.3.3 Calcitonin 176
12.4 Diuretic Effects on Calcium Transport 176
12.4.1 Role of Loop Diuretics 176
12.4.2 Thiazide Diuretics 176
12.5 Hypercalciuria 176
12.5.1 Absorptive Hypercalciuria 176
12.5.2 Renal Hypercalciuria 177
12.5.3 Resorptive Hypercalciuria 177
12.5.4 Other Forms of Hypercalciuria 177
12.6 Absorptive Hypercalciuria 178
12.6.1 Thiazides 178
12.6.1.1 Thiazides in Absorptive Hypercalciuria Type I 178
12.6.2 Slow-Release Potassium Phosphate 178
12.7 Renal Hypercalciuria 179
12.8 Primary Hyperparathyroidism 179
12.9 Dietary Recommendations Related to Calcium Metabolism 179
12.9.1 Dietary Sodium 179
12.9.2 Dietary Calcium 180
12.9.3 Calcium Supplementation 180
12.10 Conclusions 181
References 181
13: Vitamin D Metabolism and Stones 183
13.1 Introduction 183
13.2 Vitamin D Structure 184
13.3 Vitamin D Manufacture 184
13.3.1 Factors Influencing the Cutaneous Production of Vitamin D3 184
13.4 Vitamin D Metabolism 184
13.4.1 Production of 25OHD 185
13.4.2 Production of 1,25(OH)2D 185
13.4.3 Regulation of 1,25(OH)2D Production 186
13.4.4 Catabolism of 25OHD and 1,25(OH)2D 186
13.5 Biologic Actions of Vitamin D in the Intestine and Bone 186
13.5.1 1,25(OH)2D Action at the Parathyroid Gland 187
13.6 The Role of Vitamin D in the Etiology of Stone Disease 187
13.6.1 Serum Vitamin D Metabolite Concentrations in Patients with Urolithiasis 187
13.6.2 Cause for Increased 1,25(OH)2D Production 188
13.6.3 Role of the VDR in Patients with Hypercalciuria 189
13.6.4 Role of the VDR in the Genetic Hypercalciuric Stone-Forming (GHS) Rat 191
13.7 Conclusions 191
References 192
14: Urinary Citrate and Citrate Metabolism 194
14.1 Introduction 194
14.2 Physiology and Pathophysiology of Urinary Citrate in Stone Disease 194
14.3 Citrate Treatment of Stone Disease 196
14.4 Conclusions 196
References 197
15: Uric Acid Metabolism and Uric Acid Stones 198
15.1 Introduction 198
15.2 Epidemiology of Uric Acid Nephrolithiasis 198
15.3 Uric Acid Metabolism 198
15.3.1 Uric Acid Homeostasis 198
15.3.2 Renal Uric Acid Handling 199
15.3.2.1 Renal Tubular Uric Acid Reabsorption 199
15.3.2.2 Renal Tubular Uric Acid Secretion 199
15.4 Physicochemical Properties of Uric Acid 200
15.5 Etiology of Uric Acid Stones 200
15.6 Pathophysiology of Uric Acid Stones 200
15.6.1 Low Urine Volume 200
15.6.2 Hyperuricosuria 201
15.6.3 Acidic Urine pH 201
15.6.4 Impaired Ammonium Excretion 201
15.6.5 Increased Endogenous Acid Production 202
15.6.6 Role of Renal Lipotoxicity 203
15.7 Conclusions 203
References 203
16: Oxalate Metabolism and the Primary Hyperoxalurias 207
16.1 Introduction 207
16.2 Primary Hyperoxaluria 208
16.2.1 Pathophysiology 208
16.2.2 Molecular Etiology 209
16.2.2.1 Enzyme and Metabolic Defects 209
16.2.2.2 Crystal Structures of AGT and GR/HPR 209
16.2.2.3 Genes, Mutations, and Polymorphisms 209
16.2.2.4 Relationships Between Genotype and Enzyme Phenotype in PH1 210
16.2.2.5 Relationships Between Genotype and Clinical Phenotype in PH1 213
16.2.3 Diagnosis 213
16.2.4 Treatment 213
16.2.5 Treatments of the Future? 215
16.2.5.1 Chemical Chaperones 215
16.2.5.2 Hepatocyte Transplantation 215
16.2.5.3 Oxalobacter Formigenes 215
16.3 Conclusions 215
References 216
17: Cystinuria and Cystine Stones 219
17.1 Introduction 219
17.2 Epidemiology 219
17.3 Pathophysiology and Classification 219
17.3.1 Pathophysiology 219
17.3.2 Classification 220
17.4 Natural Course 221
17.5 Diagnostics and Definition 221
17.5.1 Clinical Appearance of Stones 221
17.5.2 Radiological Appearance 222
17.5.3 Urine Microscopy 222
17.5.4 24-h Urine 222
17.5.5 Definition 222
17.6 Cystine Stone Prevention 223
17.6.1 Diet 223
17.6.2 Urine Dilution 223
17.6.3 Urine Alkalinization 224
17.6.4 Medical Reduction of Cystine 224
17.7 Urological Interventions 224
17.7.1 Shockwave Lithotripsy 224
17.7.2 Ureteroscopy 224
17.7.3 PNL 225
17.7.4 Open Surgery 225
17.8 Conclusions 225
References 225
18: Urinary Infection and Struvite Stones 228
18.1 Introduction: Infection Stones 228
18.2 Bacteriology 229
18.3 Mineral Composition 230
18.4 Mechanism of Calculogenesis of Struvite Stones 231
18.5 Bacteria within the Stone and Its Significance 231
18.6 Urease and Its Role 232
18.7 Matrix in Struvite Stones and Its Role 232
18.8 Role of Urinary Stasis 232
18.9 Clinical Manifestations 233
18.9.1 Epidemiology 233
18.9.2 Clinical Presentation 233
18.10 Conclusions 234
Disclosure 234
References 234
19: Drug-Induced Renal Stones 236
19.1 Introduction 236
19.2 Mechanisms of Drug-Induced Stone Formation 236
19.3 Risk Factors Favoring Drug-Induced Stone Formation 237
19.4 Epidemiology of Drug-Induced Stones 237
19.5 Drug-Containing Renal Stones 237
19.5.1 Triamterene 237
19.5.2 Protease Inhibitors 238
19.5.3 Sulfonamides 240
19.5.4 Other Antibacterial Agents 240
19.5.5 Other Drugs 241
19.5.5.1 Magnesium Trisilicate 241
19.5.5.2 Glafenine 242
19.5.5.3 Oxypurinol, Allopurinol, and Xanthine 242
19.5.5.4 Guaifenesin, Ephedrine, and Other Stimulants 242
19.6 Metabolically Induced Renal Stones 242
19.6.1 Calcium-Containing Stones 242
19.6.1.1 Calcium and Vitamin D Supplementation 242
19.6.1.2 Carbonic Anhydrase Inhibitors 243
19.6.1.3 Furosemide 243
19.6.1.4 Antibacterial Agents in Cystic Fibrosis 244
19.6.1.5 Other Drugs 244
19.6.2 Purine-Containing Stones 244
19.6.2.1 Laxative Abuse 244
19.6.2.2 Uricosuric Drugs 244
19.6.2.3 Allopurinol 244
19.6.2.4 Urine pH Modifiers 244
19.7 Diagnosis and Prevention 245
19.8 Conclusions 245
References 245
20: Endemic Bladder Stones 249
20.1 Introduction 249
20.2 Epidemiology 249
20.3 Etiopathogenesis 250
20.4 Clinical Presentation 250
20.5 Diagnosis 250
20.6 Treatment 251
20.7 Conclusions 252
References 252
21: Economic Implications of Medical and Surgical Management 254
21.1 Introduction 254
21.2 Costs for Stone Removal (Surgical Management) 254
21.3 Costs for Metabolic Evaluation and Metaphylaxis (Medical Management) 255
21.4 Calculation Models: Comparison of Costs for Stone Removal Versus Metabolic Evaluation/Metaphylaxis 256
21.4.1 Calculation Model: Comparison of Costs for Stone Removal Versus Metabolic Evaluation/Metaphylaxis in Germany 256
21.4.1.1 Costs for Stone Removal 256
21.4.1.2 Costs for Metabolic Evaluation/Metaphylaxis 256
21.4.1.3 Comparison of Annual Costs for Stone Removal Versus Metabolic Evaluation and Metaphylaxis 257
21.4.2 Calculation Models: Comparison of Costs for Stone Removal Versus Metabolic Evaluation/Metaphylaxis in Other Countrie 258
21.5 Off Work due to Stone Disease 258
21.6 Conclusions 258
References 258
Part III Basic Sciences 260
22: What Are Shock Waves? 261
22.1 Introduction 261
22.2 Waves 261
22.2.1 Mechanical Waves 261
22.2.2 Transverse Waves 262
22.2.3 Longitudinal Waves 262
22.2.4 A Few Definitions 262
22.3 Shock Waves 264
22.3.1 Lithotripter Shock Waves 264
22.3.1.1 Shock Wave Generators 264
22.3.1.2 Shock Wave Formation 266
22.3.1.3 Parameters Describing a Lithotripter Shock Wave 266
22.3.1.4 Shock Wave Pressure Profile 267
22.3.1.5 Shock Wave Attenuation 269
22.4 Conclusions 269
References 269
23: Extracorporeal Shock Wave Lithotriptors 271
23.1 Introduction 271
23.2 Modality of Lithotripter Function 274
23.2.1 Acoustic Energy of Shock Waves 274
23.2.2 Shaping the Shock Wave Focus 275
23.3 Physical Mechanisms of Fragmentation 277
23.3.1 Spallation 277
23.3.2 Squeezing 277
23.3.2.1 Dynamic Squeezing 278
23.3.2.2 Dynamic Fatigue 278
23.4 Clinical Factors Influencing the Efficacy of Shock Waves 279
23.4.1 Propagation and Coupling 279
23.4.2 Stone Localization 279
23.4.3 Stone Positioning 280
23.4.4 Control of Shock Wave Dose 280
23.4.4.1 Pulse Rate 280
23.4.4.2 Process of Generator Voltage Along ESWL Session 280
23.4.4.3 Defining Endpoint of Shock Wave Application 281
23.4.5 Avoidance of Tissue Trauma 282
23.5 Comparison of Lithotripters 282
23.5.1 In Vitro Studies 282
23.5.2 Clinical Efficacy Quotient 282
23.5.3 Clinical Trials 282
23.5.4 Clinical Classification of Lithotripters 283
23.6 Treatment Philosophy: SWL Versus Endourology 283
23.7 Future of Shock Wave Lithotripsy 284
23.8 Conclusions 284
References 284
24: Biological Effects Produced by High-Energy Shock Waves 286
24.1 Introduction 286
24.2 Adverse Bioeffects of SWL 287
24.2.1 Renal Complications 287
24.2.1.1 Acute Effects 287
24.2.1.2 Functional Alteration 287
24.2.1.3 Chronic Effects 288
24.2.2 Effect of SWL in Pediatric Patients 289
24.2.3 Extrarenal Effects 289
24.2.3.1 Cardiovascular System 289
24.2.3.2 Lung 289
24.2.3.3 Liver 289
24.2.3.4 Pancreas 289
24.2.3.5 Bowels 290
24.2.3.6 Ureter 290
24.2.3.7 Testes and Ovaries 290
24.2.3.8 Pregnancy 290
24.3 Other Therapeutic Applications of Shock Waves 290
24.3.1 Clinical Shock Wave Therapy for Bone and Tissue Healing 290
24.3.1.1 Shock Wave Therapy for Healing of Chronic Ulcers 290
24.3.1.2 Shock Wave Therapy for Orthopedic Disorders 291
24.3.1.3 Shock Wave Therapy for Fracture Healing 291
24.3.1.4 Mechanisms of Shock-Wave-Induced Healing 291
24.3.1.5 Treatment of Peyronie’s Disease 292
24.3.2 Shock-Wave-Mediated Gene and Drug Delivery 292
24.3.2.1 Other Bioeffects of Shock Waves 293
24.4 Conclusions 294
References 294
25: Intracorporeal Nonlaser Lithotripsy 299
25.1 Introduction 299
25.2 Electrohydraulic Lithotripsy 299
25.2.1 Surgical Tips on EHL 300
25.3 Ultrasonic Lithotripsy 300
25.3.1 Surgical Tips on Ultrasonic Lithotripsy 301
25.4 Ballistic/Pneumatic Lithotripsy (Lithoclast) 301
25.4.1 Surgical Tips on Pneumatic Lithotripsy 302
25.5 Combined Pneumatic and Ultrasound Lithotripsy 302
25.5.1 Surgical Tips on Combined Pneumatic/Ultrasound Lithotripsy 303
25.6 Electrokinetic Lithotripsy 303
25.7 Contact Ballistic Lithotripsy (LMA) 303
25.8 Conclusions 304
References 304
26: Laser Lithotripsy Physics 306
26.1 Introduction 306
26.2 Laser Tissue Interaction 307
26.3 Physics of Laser Lithotripsy 309
26.4 Optical Fibers 311
26.5 Conclusions 313
References 313
27: Alternative Laser Energy Sources: Clinical Implications 315
27.1 Introduction 315
27.2 Technical Requirements for Laser Use in Endourology 315
27.3 Light–Tissue Interaction 315
27.4 Laser Emission Mode 316
27.5 Fibers 317
27.6 Individual Lasers for Stone Treatment 317
27.6.1 Photoacoustic Lasers 317
27.6.1.1 Pulsed Dye Laser 317
27.6.1.2 FREDDY Laser (Frequency-Doubled Double Pulse Nd:YAG) 318
27.6.2 Photothermal Lasers 318
27.6.2.1 Holmium:Yttrium:Aluminum:Garnet (Ho:YAG) Laser 318
27.6.2.2 Erbium:YAG laser 319
27.7 Conclusions 319
References 319
Part IV Diagnostic and Laboratory Methods 321
28: Imaging for Stones 322
28.1 Introduction 322
28.2 Techniques 322
28.2.1 Abdominal Radiograph 322
28.2.2 Intravenous Urography 323
28.2.3 Ultrasound 323
28.2.4 Computed Tomography 324
28.2.5 Magnetic Resonance Imaging 325
28.2.6 Fluoroscopic Studies 326
28.2.7 Isotope Renography 326
28.3 Establish Diagnosis of Stone Disease 326
28.3.1 Abdominal Film 326
28.3.2 Intravenous Urogram 326
28.3.3 Ultrasound 328
28.3.4 Computed Tomography 331
28.3.5 Magnetic Resonance Imaging 332
28.3.6 Fluoroscopic Studies 333
28.3.7 Isotope Renography 333
28.4 Assess Stone Burden and Distribution 333
28.5 Determine Anatomy 334
28.6 Plan Therapy 336
28.6.1 Acute Management 336
28.6.2 Elective Management 336
28.6.2.1 Stone Location 337
28.6.2.2 Stone Size/Burden 338
28.6.2.3 Stone Composition 338
28.7 Evaluate Results of Therapy 339
28.7.1 Postoperative Complications 339
28.7.2 Assess for Residual Stones 339
28.8 Evaluate Function 340
28.9 Conclusions 340
References 340
29: Urinary Stone Analysis 344
29.1 Introduction 344
29.2 Stone Components 344
29.2.1 Urinary Stone Components 344
29.2.2 Frequency of Stone Components 344
29.2.3 Morphology and Structure of Stone Components 346
29.2.3.1 Morphology 346
29.2.3.2 Texture 347
29.2.3.3 Core–Shell Relations 348
29.3 Purposes and Problems of Stone Analysis 349
29.4 Methods of Stone Analysis 349
29.4.1 Overall View of Methods of Stone Analysis 349
29.4.2 Polarization Microscopy 349
29.4.3 Infrared Spectroscopy 350
29.4.4 X-ray Diffraction 350
29.5 Evaluation of Analysis Methods 350
29.6 Conclusions 352
References 355
30: Risk Indices 357
30.1 Introduction 357
30.2 Risk Indices for Calcium Oxalate Formation 358
30.2.1 Single Quantities 360
30.2.2 Simple Ratios 360
30.2.3 Iterative Model Calculations 360
30.2.4 Complex Combined Parameters 361
30.2.5 In Vitro Crystallization Experiments with Native Urine 361
30.3 Application to a Selected Data Set 362
30.3.1 Evaluation of Single Quantities as Risk Indices 363
30.3.2 Evaluation of Simple Ratios as Risk Indices 364
30.3.3 Evaluation of Iterative Model Calculations as Risk Indices 364
30.3.4 Evaluation of Complex Combined Parameters as Risk Indices 365
30.3.5 Evaluation of In Vitro Crystallization Experiments with Native Urine 365
30.3.6 Discriminatory and Predictive Power of Selected Risk Indices 365
30.4 Benefits and Limits 367
30.5 Conclusions 367
References 368
31: Blood and Urinary Tests in Stone Formers 371
31.1 Introduction 371
31.2 Blood Tests 371
31.3 Urine Tests 372
31.4 Stone Risk Factors 373
31.4.1 Volume 373
31.4.2 Calcium 374
31.4.3 Oxalate 374
31.4.4 Citrate 374
31.4.5 Urinary pH 374
31.4.6 Uric Acid 374
31.4.7 Urinary Supersaturation 375
31.5 Dietary Risk Factors 375
31.5.1 Sodium 375
31.5.2 Potassium 375
31.5.3 Magnesium 375
31.5.4 Creatinine 375
31.5.5 Other 375
31.5.6 Loading Studies 375
31.6 Conclusions 376
References 376
32: Crystallization and Other Studies 377
32.1 Crystallization: From Solution to Solid 377
32.2 Crystallization in the Nephron 378
32.2.1 Experimental Studies Related to Crystallization in the Nephron 378
32.2.2 In Vivo Data on Crystallization in the Nephron 379
32.2.3 Data from Crystallization Experiments Related to Intratubular Events 380
32.3 Crystallization in the Interstitium 381
32.4 Stone Attached to the Papillary Surface 382
32.5 Conclusions 382
References 383
33: Experimental Models for Investigation of Stone Disease 385
33.1 Introduction 385
33.2 Induction of Hyperoxaluria 386
33.3 Calcium Oxalate Stone Formation 386
33.3.1 Crystal Formation in the Kidney 386
33.3.2 Animal Models of Stone Formation 387
33.3.3 Evaluation of Stone Formation in Different Models 387
33.4 CaOx Nephrolithiasis 389
33.4.1 Comparison Between Rat and Human Nephrolithiasis 390
33.5 Conclusions 390
References 391
34: Clinical Trials in Stone Disease 393
34.1 Introduction 393
34.2 Choice of Study Population 394
34.3 Sample Size Estimates and Assumptions 394
34.4 Baseline Assessment 398
34.5 Intervention and Concomitant Medications 399
34.6 Random Allocation 399
34.7 Participant Adherence and Compliance: Monitoring Response Variables 402
34.8 Outcome Assessment and Surrogate Endpoints 402
34.9 Issues in Data Analysis 403
34.9.1 The Intention-to-Treat Principle 403
34.9.2 Subgroup Analyses 403
34.9.3 Longitudinal Data Analysis 404
34.9.4 Interim Analysis 404
34.10 Peculiar Types of Study Design 404
34.10.1 Within-Subject Study: The Crossover Design 404
34.10.2 Additivity and Synergism: The Factorial Study 404
34.10.3 The Dose-Response Study 405
34.11 Conclusions 405
Appendix 405
Sample Size Formulas 405
Continuous Measurement (e.g., Urinary Indexes) 405
Parallel Group Design 406
Crossover Study 406
Time to Failure (i.e., Recurrence Rate) 406
References 407
Part V Pediatric Stone Disease 409
35: Epidemiology of Pediatric Urolithiasis 410
35.1 Introduction 410
35.2 Western Countries 410
35.3 Non-Western Countries 416
35.4 Conclusions 419
References 419
36: Metabolic Stone Disease in Children 422
36.1 Introduction 422
36.2 Pathophysiology 422
36.3 Clinical Presentation 424
36.4 Metabolic Factors 424
36.4.1 Hypercalciuria 424
36.4.2 Hyperoxaluria 425
36.4.3 Cystinuria 426
36.4.4 Hyperuricosuria 426
36.5 Diagnostic Evaluation 427
36.6 Treatment 428
36.6.1 Medical Treatment 428
36.6.2 Hypercalciuria 428
36.6.3 Hyperoxaluria 428
36.6.4 Uric Acid Lithiasis 428
36.6.5 Cystinuria 428
36.7 Conclusions 429
References 429
37: The Role of Minimally Invasive Techniques 432
37.1 Introduction 432
37.2 Extracorporeal Shock Wave Lithotripsy 432
37.3 Percutaneous Nephrolithotomy 434
37.4 Ureteroscopy 436
37.5 Conclusions 438
References 438
Part VI Surgical Management I 440
38: Indications for Surgical Removal, Including Asymptomatic Stones 441
38.1 Preoperative Evaluation 441
38.1.1 Indications for Treatment of Stones 442
38.1.2 Asymptomatic Stones and Treatment 442
38.1.3 Asymptomatic Stones: Staghorn Calculi 443
38.2 Treatment Options 443
38.2.1 Extracorporeal Shock Wave Lithotripsy 443
38.2.1.1 Failure to Transmit Sufficient Energy to the Stone 444
38.2.1.2 Large Stone Size 444
38.2.1.3 Failure of Stone Fragmentation and Passage of Fragments 444
38.2.1.4 The Success Rates of SWL 444
38.2.2 Flexible and Rigid Ureterorenoscopy 445
38.2.3 Percutaneous Nephrolithotomy 446
38.2.4 Laparoscopic Nephrolithotomy and Ureterolithotomy 447
38.3 Conclusions 447
References 449
Part VII Extracorporeal Shock Wave Lithotripsy 452
39: Renal Stones 453
39.1 Introduction 453
39.2 Physics of SWL 453
39.3 Imaging 454
39.3.1 Fluoroscopy 454
39.3.2 Ultrasonography 454
39.3.3 Combination of Ultrasonography and Fluoroscopy 454
39.4 Anesthesia 454
39.5 Indications 455
39.6 Contraindications 455
39.7 Complications of SWL 456
39.7.1 Immediate Complications 456
39.7.1.1 Complications Related to Stone Fragments 456
39.7.2 Infectious Complications 457
39.7.3 Tissue Damage Through Shock Waves 458
39.7.3.1 Acute Renal Injury 458
39.7.3.2 Extrarenal Injury 458
39.7.4 Delayed Complications 458
39.7.4.1 Chronic Renal Injury 458
39.7.4.2 Fertility 458
39.8 Predictive Clinical Outcome Factors 458
39.8.1 Stone Position 459
39.8.2 Stone Burden 459
39.8.3 Stone Composition/Density 460
39.8.4 Renal Abnormalities and SWL 460
39.8.5 Obesity and SWL 460
39.9 Improving the Success Rate of SWL 460
39.9.1 Shock-wave Rate 460
39.9.2 Adjuvant Drug Therapy 460
39.9.3 Percussion, Diuresis, and Inversion (PDI) Therapy 461
39.10 Success Rates of SWL 461
39.10.1 Stone Size (Largest Diameter) 461
39.10.2 Stone Site 461
39.10.3 Stone Number 461
39.10.4 Obstruction 461
39.10.5 Congenital Anomalies 461
39.11 Special Considerations in SWL 461
39.11.1 SWL for Uric Acid Stones 461
39.11.2 SWL in Children 462
39.11.3 SWL in Pregnancy 462
39.11.4 Pacemakers and Implantable Cardioverters/Defibrillators (ICD) 462
39.12 Conclusions 462
References 462
40: Extracorporeal Shock Wave Lithotripsy for Ureteral Stones 466
40.1 Introduction 466
40.2 Indications and Contraindications 466
40.2.1 Indications 466
40.2.2 Contraindications 467
40.3 Factors Impacting Outcomes of SWL for Ureteral Calculi 467
40.3.1 Intrinsic Factors 467
40.3.1.1 Stone Size 467
40.3.1.2 Composition 468
40.3.1.3 Stone Location 468
40.3.1.4 Impacted/Obstructing Ureteral Calculi 468
40.3.2 Patient Factors 469
40.3.2.1 Body Habitus 469
40.3.2.2 Patient Positioning and Stone Localization 469
40.3.3 Extrinsic Factors 470
40.3.3.1 Type of Lithotriptor 470
40.3.3.2 Treatment Parameters 470
40.3.3.3 Adjuvant Medical Therapies 470
40.4 Clinical Efficacy 471
40.4.1 Stone-Free Rates 472
40.5 Complications and Side Effects 472
40.6 Additional Considerations 472
40.6.1 Quality of Life 472
40.6.2 Cost 472
40.6.3 Retreatment by SWL 473
40.7 Conclusions 473
References 473
Part VIII Surgical Management II: Endoscopy 475
41: Percutaneous Nephrolithotomy 476
41.1 Introduction 476
41.2 Anatomical Considerations 476
41.3 Preoperative Assessment 478
41.3.1 Imaging 478
41.3.2 Patient Assessment 478
41.3.3 Anesthetic Considerations 478
41.4 PCNL: Operative Technique 478
41.4.1 Ureteric Catheter Placement 478
41.4.2 Antegrade Needle Access 479
41.4.3 Urologist or Radiologist? 479
41.4.4 Fluoroscopy or Ultrasound? 479
41.4.5 Percutaneous Puncture: Fluoroscopic Approach 479
41.4.6 Tract Dilatation: Placing the Guidewire 481
41.4.7 Serial Dilators 481
41.4.8 Balloon Dilatation 482
41.4.9 The “Mini-Perc” 482
41.5 Stone Clearance: Tricks of the Trade 483
41.6 Nephrostomy 483
41.7 Complications 485
41.8 Special Situations 486
41.8.1 Bilateral Stone Disease 486
41.8.2 Ectopic Kidneys 486
41.8.3 Horseshoe Kidneys 486
41.8.4 Obesity 487
41.8.5 Pediatric PCNL 487
41.9 Conclusions 488
References 488
42: Ureteroscopy for Ureteric Stones 491
42.1 Introduction 491
42.2 Ureteral Calculi 492
42.3 Distal Ureteral Stones 492
42.4 Upper/Proximal Ureteral Stones 494
42.5 Stone Retrieval Devices 496
42.6 Intracorporeal Lithotrites 497
42.7 Assistive Devices 497
42.8 Complications of Ureteroscopy 498
42.9 Conclusions 499
References 499
43: Indications for and Technique of Retrograde Intrarenal Surgery for Renal Stones 502
43.1 Introduction 502
43.2 Differential Indications for Renal Stone Treatments 502
43.3 The Evolution of Upper Tract Endoscopy and RIRS 503
43.4 Current Indications for RIRS 503
43.5 Preparation for Surgery 504
43.5.1 Patient Preparation 504
43.5.2 Anesthesia 504
43.5.3 Equipment and Instruments 505
43.5.4 Procedure Considerations 506
43.6 Upper Urinary Tract Access for RIRS 506
43.6.1 Technique 506
43.6.2 Upper Urinary Tract Dilation 506
43.7 Flexible Ureterorenoscopy: Technique 507
43.8 Retrograde Intrarenal Surgery (RIRS) 507
43.8.1 Stone Fragmentation: Electrohydraulic and Laser Technology 507
43.8.2 Stone Composition 508
43.8.3 Renal Pelvis Stones 508
43.8.4 Calyceal Stones 509
43.8.5 Stones Associated with Intrarenal Stenosis and Calyceal Diverticula 509
43.9 Anatomical Abnormalities 511
43.9.1 Solitary Kidney 511
43.9.2 Pelvic Kidney 511
43.9.3 Transplant Kidney 511
43.9.4 Fused/Ectopic Kidney 513
43.9.5 Obese Patients 513
43.9.6 Skeletal Abnormalities 513
43.9.7 Upper Tract Reconstruction 513
43.10 Complications of RIRS 513
43.10.1 Prevention 513
43.10.2 Management 515
43.11 Conclusions 515
References 516
44: Urolithiasis in Pregnancy 517
44.1 Introduction 517
44.2 General Effects of Pregnancy on the Urinary Tract 518
44.3 Fetal Considerations in the Management of Urolithiasis in Pregnancy 518
44.3.1 Radiation Exposure 518
44.3.2 Analgesics and Antibiotics 519
44.4 Clinical Presentation 520
44.5 Choice of Imaging Modalities 520
44.5.1 Ultrasound (US) 521
44.5.2 MR Urography (MRU) 521
44.5.3 Intravenous Urogram (IVU) 521
44.5.4 Computed Tomography (CT) 521
44.5.5 Radionuclide Renography 522
44.6 Clinical Management Options 522
44.6.1 Conservative Treatment 522
44.6.2 Surgical Treatment 522
44.6.2.1 Percutaneous Nephrostomy 523
44.6.2.2 Ureteral Stent 523
44.6.2.3 Ureteroscopy 523
44.6.3 Algorithm for the Management of Stone Disease in Pregnant Women 523
44.6.4 Pregnancy Outcome and Complications 524
44.6.5 Clinical Management of Asymptomatic Stones in Patients Contemplating Pregnancy 525
44.7 Conclusions 526
References 526
45: Surgical Management of Urolithiasis in Transplanted Kidneys 529
45.1 Introduction 529
45.2 Donated Kidney 529
45.3 De Novo Formation 530
45.4 Clinical Manifestations 530
45.5 Treatment 531
45.5.1 Observation 531
45.5.2 Shockwave Lithotripsy 531
45.5.3 Ureteroscopy 532
45.5.4 Percutaneous Nephrostolithotomy 532
45.6 Conclusions 533
References 533
46: Stents and Stenting 535
46.1 Introduction 535
46.2 History of Stents 535
46.3 Stents: Design and Materials 536
46.3.1 Stent Materials 536
46.3.2 Stent Design 537
46.3.2.1 Grooved Stents 537
46.3.2.2 Spiral Stents 537
46.3.2.3 Meshed Stents 537
46.3.2.4 Tail Stents 537
46.3.2.5 Dual-Durometer Stents 537
46.3.2.6 Magnetic-Tipped Stents 537
46.3.2.7 Other Designs 538
46.3.3 Stent Coatings 538
46.4 Indications 538
46.4.1 Stent Use in SWL 539
46.4.2 Stents for Drainage 539
46.4.3 Stents Post-ureteroscopy 539
46.5 Complications 540
46.6 Recent Advances 541
46.6.1 Drug-Eluting Stents 541
46.6.2 Tissue-Engineered Stents 541
46.7 Conclusions 541
References 542
47: Flexible Ureterorenoscopy: Tips and Tricks 544
47.1 Introduction 544
47.2 Theater Setup and Patient Positioning 544
47.2.1 General Layout of the Operating Theater 544
47.2.2 Position of the Surgeon 545
47.2.3 Positioning the Patient in the Lateral Decubitus Position 545
47.2.4 Positioning the Patient in the Trendelenburg Position 545
47.2.5 Operating Table, Guide Wire, and Laser Unit 545
47.2.6 Setup of the Operating Area 547
47.2.7 Irrigation Tube, Optic, and Camera 548
47.3 Irrigation Techniques 548
47.4 Different Possible Configurations for Irrigation in Flexible Ureterorenoscopy 549
47.4.1 Hydrostatic Pressure 549
47.4.2 Manual High Pressure 549
47.4.3 Pressure Cuff 549
47.4.4 High Pressure with a Syringe 550
47.4.5 Automatic High-Pressure Machine 551
47.5 Insertion of the Safety Guide Wire 551
47.5.1 Use of a Cystoscope 551
47.5.2 Use of a Dual-Lumen Catheter 551
47.5.3 Use of a Ureteral Access Sheath 552
47.6 Insertion of the Ureterorenoscope into the Ureteral Meatus 553
47.7 Insertion of the Ureteral Access Sheath 554
47.7.1 Roles and Advantages of the UAS 554
47.7.2 Insertion of the Ureteral Access Sheath 554
47.8 Examination of the Renal Caliceal Cavities 555
47.8.1 Neutral Position of the Dominant Hand (Right Hand) 555
47.8.2 Examination of Right Renal Caliceal Cavities: Dominant Right Hand in Supination 555
47.8.3 Examination of Left Renal Caliceal Cavities: Dominant Right Hand in Pronation 555
47.9 Ureterorenoscope and Laser: Working Channel, Instrumentation, and Synergy Laser-Ureterorenoscope 556
47.9.1 The Holmium-YAG Laser 557
47.9.2 Laser Fiber Not Fixed by Seal (Not Recommended) 557
47.9.3 Laser Fiber Fixed by Seal (Strongly Recommended) 557
47.10 Management of Lower-Pole Calculi 557
47.11 Fragmentation Techniques, Clotting Technique 558
47.11.1 Fragmentation in a Stone Blocked Against a Renal Papillae 559
47.11.2 “Postage Stamp” Fragmentation Technique 559
47.11.3 Clotting Technique 559
47.12 Stone Removal Techniques 559
47.12.1 Removal by “Trapping” Stone on the Ureteral Access Sheath 560
47.12.2 Release of a Stone Captured in a Nitinol Basket 560
47.12.3 Captured Stone Hemmed-In in the Ureter, Nitinol Basket in Place 560
47.13 Prevention of Stone Fragment Accumulation in Lower Calyx 562
47.14 Management of Caliceal Diverticula 562
47.15 Retrograde Endopyelotomy 562
47.16 Antegrade Flexible Ureteroscopy 562
47.17 Management of Urothelial Tumors 565
47.18 Conclusions 566
References 566
48: Training Implications for Stone Management 568
48.1 Introduction 568
48.2 History of Surgical Training and Impact of Endourologic Teaching 569
48.3 Creating the Curriculum for Teaching Endourology 570
48.3.1 Learning with Practice 570
48.3.2 New Developments in Urinary Stone Disease Education Strategies 571
48.4 Material-Based Models 571
48.5 Animals 573
48.6 Cadaveric Anatomic Materials 573
48.7 Simulators for Teaching Endourology 574
48.8 Assessment and Maintenance of Certification 575
48.9 Conclusions 575
References 575
Part IX Surgical Management III: Open Surgery 579
49: Open Surgery to Remove Stones: When and How? 580
49.1 ..Introduction 580
49.2 Indications for Open Stone Surgery 580
49.3 Preoperative Diagnostics 582
49.3.1 Sonography 582
49.3.2 Plain X-ray and Intravenous Urography 582
49.3.3 CT Scan 582
49.3.4 Scintigraphy 582
49.3.5 Urine Culture 582
49.4 Surgical Techniques for Open Stone Removal 583
49.4.1 Approach 583
49.4.2 Cold Ischemia 583
49.4.3 Simple Pyelolithotomy 583
49.4.4 Extended Pyelolithotomy (Gil-Vernet) 584
49.4.5 Pyelonephrolithotomy 584
49.4.6 Anatrophic Nephrolithotomy 585
49.4.7 Radial Nephrotomy 585
49.4.8 Partial Nephrectomy 586
49.5 Conclusions 587
References 588
50: Autotransplantation and Ureteric Replacement: In Whom and How? 590
50.1 Introduction 590
50.2 Indications and Contraindications 590
50.3 Operative Technique 591
50.3.1 Ileal Ureter 591
50.3.2 Boari Flap 592
50.3.3 Renal Autotransplant 592
50.3.4 Yang-Monti 594
50.3.5 Appendix 594
50.4 Results 594
50.4.1 Ileal Ureter 594
50.4.2 Boari Flap 595
50.4.3 Renal Autotransplant 595
50.4.4 Yang-Monti 595
50.4.5 Appendix 595
50.5 Complications 604
50.6 Conclusions 604
References 604
51: Liver and Renal Transplantation in Primary Hyperoxaluria 606
51.1 Introduction 606
51.2 Clinical Management 607
51.3 Transplantation 607
51.3.1 Isolated Renal Transplantation 607
51.3.2 Combined Liver/Kidney Transplantation 608
51.3.2.1 Timing of Transplantation 609
51.3.3 Liver Transplantation Alone 609
51.3.4 Other Forms of Transplantation 610
51.3.4.1 Sequential Transplantation 610
51.3.4.2 Auxiliary Liver Transplantation 610
51.3.5 Transplantation in PH2 610
51.3.6 Postoperative Supportive Therapy 610
51.4 Our Experience So Far: The European PH1 Transplant Registry 610
51.4.1 Patients 611
51.4.2 Results/Outcomes 611
51.5 Conclusions 612
References 613
52: Chemolytic Treatment of Patients with Urinary Tract Stones 615
52.1 Introduction 615
52.2 Chemolytic Treatment of Patients with Infection Stones 616
52.3 Cystine Stone Dissolution 618
52.4 Dissolution of Stones Composed of Uric Acid 620
52.5 Calcium Phosphate 623
52.6 Calcium Oxalate 623
52.7 Conclusions 624
References 624
Part X Medical Management 626
53: Establishment and Management of a Stone Clinic 627
53.1 Introduction 627
53.2 Stone Clinic 627
53.3 Screening for the Risk of Stone Formation 630
53.3.1 Patientscreen 630
53.3.2 Stonescreen 632
53.3.3 Metascreen 632
53.3.4 Urinescreen 633
53.3.5 Dietscreen 633
53.4 Epidemiological Factors in the Formation of Urinary Stones 633
53.5 Prevention of Stone Recurrence 634
53.6 Conclusions 635
References 636
54: Medical Expulsive Therapy 637
54.1 Introduction 637
54.2 Effect of Pharmacological Agents on Ureteral Function 637
54.2.1 Calcium Channel Antagonists 638
54.2.2 Alpha-1A-Adrenoceptor Antagonists 639
54.2.3 Direct Comparison between Nifedipine and Tamsulosin 641
54.2.4 Meta-Analysis of Clinical Trials Using Tamsulosin or Nifedipine 641
54.2.5 The Role of Steroids 641
54.3 Conclusions 642
References 642
55: Metabolic Investigations: When and in Whom 645
55.1 Introduction 645
55.2 Evaluation of Stone Formers 646
55.2.1 History 646
55.2.2 Laboratory Evaluation 647
55.3 Twenty-Four Hour Urine Collections 647
55.4 Conclusions 650
Disclosure 650
References 650
56: Medical Management of Idiopathic Calcium Stone Disease 652
56.1 Introduction 652
56.2 Dietary Factors 652
56.2.1 Fluids 652
56.2.2 Sodium 653
56.2.3 Animal Protein 653
56.2.4 Fruits and Vegetables 653
56.2.5 Dietary Calcium 653
56.2.6 Dietary Oxalate 654
56.3 Pharmacological Therapy 654
56.3.1 Thiazides 655
56.3.2 Potassium Citrate 655
56.3.3 Allopurinol 656
56.3.4 Orthophosphates 656
56.4 Conclusions 656
References 656
57: Medical Management: Uric Acid and Cystine Stones 658
57.1 Introduction 658
57.2 Uric Acid 658
57.2.1 Clinical Presentation 658
57.2.2 Diagnosis 659
57.2.3 Differential Diagnosis 659
57.2.4 Treatment 659
57.2.4.1 Lifestyle Modifications 659
57.2.4.2 Specific Pharmacological Treatment 659
57.3 Cystine 660
57.3.1 Clinical Presentation 660
57.3.2 Diagnosis 660
57.3.3 Physicochemistry of Cystine 661
57.3.4 Treatment 661
57.3.4.1 Lifestyle Modifications 661
57.3.5 Specific Pharmacological Treatment 662
57.3.5.1 Oral Alkali Treatment 662
57.3.5.2 Chelating Agents 663
57.3.6 Other Pharmacological Treatments 664
57.4 Conclusions 664
References 664
58: Medical Management of Struvite Stones 666
58.1 Introduction 666
58.2 Pathogenesis 666
58.3 Bacteriology 667
58.4 Epidemiology – Clinical Manifestations 667
58.5 Medical Management 668
58.5.1 Dissolution Therapy (Chemolysis) 668
58.5.2 Urease Inhibitors 669
58.5.3 Acidification 669
58.5.4 Antimicrobials 669
58.5.5 Diet 670
58.6 Conclusions 670
References 670
59: Dietary Assessment and Advice 672
59.1 Introduction 672
59.2 Dietary Assessment 672
59.3 General Dietary Metaphylaxis 673
59.4 General Recommendations for Fluid Intake 673
59.5 Calcium Oxalate Stone Disease 674
59.5.1 Hyperoxaluria 674
59.5.2 Hypercalciuria 675
59.5.3 Hyperuricosuria 675
59.5.4 Hypocitraturia and Hypomagnesuria 675
59.6 Uric Acid Stone Disease 675
59.6.1 Hyperuricosuria 675
59.6.2 Low Urinary pH 676
59.6.3 Low Urine Volume 676
59.7 Calcium Phosphate Stone Disease 676
Sec15_59 676
59.7.1 Hypercalciuria 676
59.7.2 Hyperphosphaturia 677
59.7.3 High Urinary pH 677
59.8 Cystine Stone Disease 677
59.8.1 Cystinuria 677
Sec21_59 677
59.8.2 Low Urine Volume 677
59.9 Conclusions 677
References 678
60: Stone Management in the Presence of Morbid Obesity 680
60.1 Introduction 680
60.2 Epidemiology of Obesity 680
60.2.1 Obesity in the United States 680
60.2.2 Obesity Worldwide 681
60.2.3 Obesity in Children and Adolescents 681
60.3 Epidemiology of Stones in the Obese Population 681
60.3.1 Calcium Oxalate and Uric Acid Stones 681
60.4 Risk Factors for Stones in the Obese Population 681
60.4.1 General Risk Factors 681
60.4.2 Urinary Metabolic Factors 682
60.4.3 Dietary Risk Factors 682
60.4.4 Mechanism 682
60.5 Conservative Therapy for Stone Disease 683
60.5.1 Medication 683
60.5.2 Diet 684
60.5.3 Imaging in Obesity 684
60.5.4 Bariatric Surgery and Stone Disease 685
60.6 Surgical Therapy for Stone Disease 686
60.6.1 General Considerations 686
60.6.2 Extracorporeal Shock Wave Lithotripsy (SWL) 686
60.6.3 Ureteroscopy 687
60.6.4 Percutaneous Nephrolithotomy (PCNL) 688
60.6.5 Recent Developments in Endourology in Obesity 688
60.7 Conclusions 689
References 689
Index 692