Comprehensive Frontier of Kidney Disease (in 2 Volumes) (Dec 17, 2024)_(9811286035)_(World Scientific Publishing Company)

"In a world where kidney injury poses an ever-growing threat to human health due to aging populations and changing lifestyles, understanding and combating renal diseases have never been more critical. This book delves into cutting-edge renal disease research, where rapid developments have illuminated new technologies for diagnosis and treatment of the disease. The book systematically and comprehensively addresses clinical issues related to kidney diseases, where readers can explore topics such as hypoxia-inducible factors and renal anemia, pathogenesis of IgA nephropathy, hypertension, diabetic nephropathy, PLA2R antibodies and membranous nephropathy, immune nephropathy treatments using biological agents, renal glucose and energy metabolism, the application of SGLT2 inhibitors, and mechanisms of renal fibrosis. Written by over thirty experts who are actively shaping the field of nephrology in China and the USA, this book offers profound insights to understanding renal diseases, making it an indispensable resource for researchers, clinicians, and readers seeking to grow their knowledge on the scientific issues of kidney disease"-- Provided by publisher Volume 1 Contents Foreword Preface About the Editors Part 1. Chronic Kidney Disease Chapter 1. Epidemiology and Economic Burden of CKD in China 1.1 Introduction 1.2 Epidemiology of CKD 1.2.1 Prevalence of CKD 1.2.2 Awareness of CKD 1.2.3 Evolving spectrum of CKD 1.2.4 Traditional and novel risk factors of CKD 1.2.5 Clinical outcomes of CKD 1.3 Economic Burden of CKD 1.4 Burden of ESKD 1.5 Research Needs Regarding the Epidemiology of CKD References Chapter 2. Comprehensive Understanding of Kidney Disease and Hypertension 2.1 Introduction 2.2 Renal Artery Stenosis 2.3 Guyton’S Pressure Natriuresis Theory 2.4 “Osmotically Inactive Sodium” Accumulation and Hypertension 2.5 Skin Sodium and Hypertension 2.5.1 Tissue macrophages and lymphatic vessels on sodium balance, interstitial volume, and blood pressure 2.5.2 Possible factors affecting skin “Nonosmotic Sodium” accumulation and blood pressure 2.5.3 Skin capillary density 2.5.4 The hypoxia inducible factor (HIF) transcription system 2.6 Hypertension and Immunity and Inflammation 2.6.1 Involvement of the innate/adaptive immune system in the pathogenesis of hypertension 2.6.2 Role of “Autoantigens” in the pathogenesis of immune activation and hypertension 2.6.3 Relationship between salt, the immune system and hypertension 2.7 Renal Nerves and Hypertension 2.8 Conclusion References Chapter 3. Renal Anemia: The Role of Hypoxia-Inducible Factor-Prolyl Hydroxylase Inhibitor 3.1 Introduction 3.2 HIF Transcription Factors 3.3 HIF Biology 3.4 HIF in Erythropoiesis 3.5 HIF-PHD Inhibitor in Clinical Trials 3.5.1 Patients with DD–CKD 3.5.2 Patients with NDD–CKD 3.5.3 Patients of anemia with inflammation 3.5.4 Other specific populations 3.6 Benefits of HIF-PHI Therapy 3.6.1 Stimulation of endogenous EPO 3.6.2 Improvement in iron metabolism 3.6.3 Other benefits 3.7 Safety 3.7.1 Cardiovascular safety 3.7.2 Potential carcinogenic 3.7.3 Other safety considerations 3.8 Conclusion References Chapter 4. Klotho and Chronic Kidney Disease 4.1 Introduction 4.2 Overview of Anti-aging Gene Klotho 4.2.1 Structural features of Klotho protein 4.2.2 Biological role of Klotho 4.2.2.1 Membrane-bound Klotho protein 4.2.2.2 Circulating Klotho protein 4.3 Klotho Protein and CKD 4.3.1 Characteristics of changes in Klotho protein within CKD patients 4.3.2 Klotho protein and kidney protection 4.3.3 Klotho protein and CKD–MBD 4.4 Klotho and Cardiovascular Complications of CKD 4.4.1 Klotho protein and VC 4.4.2 Klotho protein and LVH 4.4.3 Klotho protein and CKD-accelerated AS 4.4.3.1 Prevention and treatment of vascular endothelial dysfunction 4.4.3.2 Prevention and treatment of VSMC damage 4.4.3.3 Inhibition of monocyte/macrophage activation 4.4.3.4 Inhibition of abnormal platelet activation 4.5 Prospects for Clinical Application of Klotho in CKD 4.5.1 As a new biomarker for CKD 4.5.2 As a new prevention and treatment strategy for CKD 4.5.2.1 Regulation of endogenous Klotho expression 4.5.2.2 Exogenous supplementation of Klotho protein References Chapter 5. Role of SGLT2 Inhibitor in Cardiorenal Protection with DKD: New Perspectives 5.1 Introduction 5.2 SGLTs and SGLT2 Inhibitors 5.2.1 The classification and distribution of SGLTs 5.2.2 The function of SGLT2 and SGLT2 inhibitors 5.3 Cardiorenal Benefits of SGLT2 Inhibitors in DKD 5.3.1 Cardiovascular benefits of SGLT2 inhibitors in clinical trials 5.3.2 Renal benefits of SGLT2 inhibitors in clinical trials 5.4 Mechanisms of SGLT2i in Mediating Cardiorenal Protection 5.4.1 Improving glycemic control 5.4.2 Osmotic diuresis and natriuresis 5.4.3 Lowering BP 5.4.4 Reducing body weight 5.4.5 Inhibiting the sympathetic nervous system 5.4.6 Inhibiting myocardial Na+/H+ exchange 5.4.7 Reducing inflammation and oxidative stress 5.4.8 Mimicking hypoxia and stimulating erythropoiesis 5.4.9 Increased ketogenesis 5.4.10 Effects on metabolic reprogramming 5.5 Conclusion References Chapter 6. Mineralocorticoid Receptor: An Old Target But New Evidence 6.1 Introduction 6.2 The Physiology and Pathophysiology of Aldosterone and MR 6.3 The Development History of MRAs 6.4 MRA and CKD 6.5 Conclusion References Part 2. Glomerular Disease Chapter 7. The Immunological Mechanism Involved in Primary Glomerular Diseases 7.1 Introduction 7.2 Immune Cells in the Kidney 7.3 Innate Immunity in Glomerular Diseases 7.3.1 Damage-associated molecular patterns and pattern recognition receptors 7.3.2 The complement system 7.3.3 MicroRNAs 7.4 Adaptive Immunity of Glomerular Diseases 7.4.1 T cell immune response 7.4.2 B cell immune response 7.5 Advances in Immune-based Therapies for Primary Glomerular Diseases 7.5.1 Complement-directed therapies 7.5.2 B cell-targeting therapies 7.6 The Effect of Glomerular Disease on the Immune System 7.7 Conclusion References Chapter 8. Membranous Nephropathy: New Mechanisms and Therapies 8.1 Introduction 8.2 Contribution of Heymann Nephritis in the Understanding of MN 8.3 The Role of Complement in MN 8.4 MN Associated Autoantigens in Humans 8.5 Clinical Significance of Serum PLA2R Antibody 8.5.1 Can measurement of PLA2R antibodies be used to diagnose MN? 8.5.2 Can PLA2R positive be used to exclude secondary causes of MN? 8.5.3 Can PLA2R antibody levels guide treatment decisions? 8.6 Treatment of PrimaryMN 8.6.1 Supportive cares 8.6.2 Initiation of IS therapy 8.6.3 IS regimens 8.7 Diagnosis and Treatment Experience in Huashan Hospital 8.8 Summary and outlook References Chapter 9. New Insights Into the Mechanism of Edema Formation in Nephrotic Syndrome: The Role of Plasmin and its Clinical Implication 9.1 Introduction 9.2 The Hypothetic Mechanisms of Edema in NS 9.2.1 Underfill hypothesis 9.2.2 Overfill hypothesis 9.2.3 Plasmin and its role in Epithelial Na channel (ENac) activation 9.3 Clinical Implications 9.3.1 Plaminuria and inhibition of plasmin-induced activation of ENaC 9.3.2 Management of edema 9.3.3 Management of hypertension 9.4 Conclusion References Chapter 10. What’s New on IgA Nephropathy: Pathogenesis and Therapies 10.1 Introduction 10.2 Pathogenesis 10.2.1 Mucosal immune system and IgA nephropathy 10.2.2 Complement activation in IgA nephropathy 10.3 Therapies 10.3.1 Supportive therapy 10.3.1.1 Sodium-glucose cotransporter-2 inhibitors (SGLT2i) 10.3.1.2 Endothelin receptor antagonists 10.3.2 Corticosteroids therapy 10.3.2.1 Systemic corticosteroids therapy 10.3.2.2 Targeted-release corticosteroids therapy 10.3.3 Toll-like Receptor (TLR) inhibitor 10.3.4 Emerging treatment approaches and experimental therapies 10.3.4.1 Complement inhibitors 10.3.4.2 Targets in B cell maturation 10.4 Conclusion References Chapter 11. Lupus Nephritis: Research Highlights and Progress of Treatment 11.1 Introduction 11.2 Progress in the Pathogenesis of LN 11.2.1 Genetic background [2] 11.2.2 Innate immunity 11.2.3 Adaptive immunity 11.2.4 LN and B cells 11.2.4.1 Development and homeostasis of normal B cells 11.2.4.2 The role of abnormal B cell tolerance and regulation in the pathogenesis of LN 11.2.4.3 The significance of targeting BLyS in the treatmentof LN 11.3 Update of Diagnostic Criteria for LN 11.3.1 Clinical diagnostic criteria 11.3.2 Pathological diagnostic criteria for LN 11.4 Treatment 11.4.1 Targeted B cell therapy 11.4.2 Novel targeted therapy 11.5 Conclusion References Chapter 12. Diabetic Kidney Disease: A New Horizon 12.1 Introduction 12.2 Definition and Diagnosis of Diabetic Kidney Disease (DKD) 12.2.1 Definition of DKD 12.2.2 Significance of microalbuminuria in the diagnosis of DKD 12.2.3 Differential diagnosis for DKD 12.3 Treatment Strategies for DKD 12.3.1 Lifestyle improvement 12.3.2 Control blood sugar 12.3.2.1 Blood sugar control target 12.3.2.2 Choice of hypoglycemic drugs 12.3.2.3 SGLT-2 inhibitor 12.3.2.4 Glucagon-like peptide 1 receptor agonist (GLP-1 RA) 12.3.2.5 Dipeptidyl peptidase-4 (DPP-4) inhibitors 12.3.3 BP control 12.3.3.1 BP control goals 12.3.3.2 Selection of antihypertensive drugs 12.3.4 Mineralocorticoid receptor antagonists 12.3.5 Correct lipid disorder 12.4 Outlook for DKD Treatment References Chapter 13. Applications of Recent Innovations in Renal Pathology 13.1 Introduction 13.2 New Technologies 13.2.1 Different omics on the basis of kidney tissue 13.2.1.1 Genomics 13.2.1.2 Transcriptomics 13.2.1.3 Proteomics 13.2.2 Digital pathology and artificial intelligence 13.3 New Concepts 13.3.1 Transition from a purely morphological diagnosis to a diagnosis that combines both morphology and etiology 13.3.2 Transition from description and semi-quantitative analysis to fully quantitative analysis 13.3.3 Transition from working alone to creating a collaborative environment 13.3.3.1 European Renal cDNA Bank–Kröner Fresenius BiopsyBank (ERCB–KFB) 13.3.3.2 Clinical Phenotyping Resource and Biobank Core (C-PROBE) 13.3.3.3 Nephrotic Syndrome Study Network (NEPTUNE) 13.3.3.4 Kidney Precision Medicine Project (KPMP) 13.4 Clinical Applications 13.4.1 Precision diagnosis and evaluation 13.4.2 Precision treatment 13.4.3 Drug discovery 13.5 Conclusion References Chapter 14. Biologic Agents in the Treatment of Glomerular Diseases: Current Status and Future 14.1 Introduction 14.2 Targeting Immune Cells 14.2.1 Anti-CD20 monoclonal antibodies 14.2.2 Anti-CD38 monoclonal antibodies 14.2.3 Blocking B cell survival factors 14.2.4 Targeting T cells 14.3 Targeting Complement System 14.3.1 Blocking C5/C5a in the terminal pathway 14.3.2 Inhibitors of factor B and factor D in the alternative pathway 14.3.3 Monoclonal antibody against MASP-2 in the lectin pathway 14.4 Targeting Inflammatory Pathway 14.4.1 Anti-IL-5 and anti-IL-5R monoclonal antibodies 14.4.2 Anti-IL-6 monoclonal antibody 14.4.3 Anti-IFN-I receptor monoclonal antibody 14.4.4 Biologics targeting others cytokines 14.5 Challenges and future Future Directions 14.6 Conclusion References Part 3. Acute Kidney Injury Chapter 15. Acute Kidney Injury: From Bench to Bedside 15.1 Introduction 15.2 Susceptibility to AKI 15.3 Biomarkers of AKI 15.4 Prediction of AKI 15.5 Prevention and Treatment of AKI 15.6 Post-AKI Care 15.7 Conclusion References Chapter 16. Sepsis and AKI: Pathogenesis and Therapies 16.1 Introduction 16.2 Pathogenesis of Sepsis and Septic AKI 16.3 Rational of Blood Purification for Sepsis 16.3.1 “Cytokine peak” hypothesis 16.3.2 “Threshold immunomodulation” hypothesis 16.3.3 “Mediator delivery” hypothesis 16.3.4 “Cytokinetic model” hypothesis 16.4 Extracorporeal Blood Purification Therapies for Sepsis 16.4.1 High-volume hemofiltration 16.4.2 Coupled plasma hemofiltration adsorption 16.4.3 High cut-off hemofiltration 16.4.4 Polymyxin B adsorption 16.4.5 Oxiris membrane 16.4.6 CytoSorb 16.5 Novel Blood Purification Therapies for Septic AKI 16.5.1 Cell therapy 16.5.1.1 Artificial renal tubular epithelial cell system 16.5.1.2 Extracorporeal cell therapy with granulocytes 16.5.1.3 Endothelial bioreactor system 16.5.2 Cell processing 16.5.2.1 Granulocyte adsorption 16.5.2.2 FcMBL hemoadsorption filter 16.6 Conclusion References Chapter 17. Autophagy and Acute Kidney Disease 17.1 Introduction 17.1.1 Acute kidney injury and acute kidney disease 17.1.2 Autophagy in AKD 17.1.2.1 The molecular basis of autophagy 17.1.2.2 Main regulatory signaling pathways of autophagy 17.1.2.3 Selective autophagy 17.2 Autophagy in AKI 17.2.1 Autophagy in ischemic AKI 17.2.2 Autophagy in cisplatin-induced nephrotoxic AKI 17.2.3 Autophagy in response to sepsis 17.3 Autophagy in Kidney Repair after AKI 17.4 Conclusion and Prospects References Chapter 18. Current Understanding of the Transition of AKI to CKD 18.1 Introduction 18.2 Animal Model of AKI-to-CKD Transition 18.2.1 Development of AKI to CKD model by IR 18.2.2 Development of AKI to CKD model by UUO 18.2.3 Development of AKI to CKD model by nephrotoxic toxin 18.3 Understanding of AKI-to-CKD Transition 18.3.1 Inflammatory cells associated with AKI-to-CKD transition 18.3.1.1 Neutrophils 18.3.1.2 Mononuclear macrophages 18.3.1.3 Dendritic cells (DCs) 18.3.1.4 Lymphocytes 18.3.1.5 Renal tubular epithelial cells 18.3.1.6 Endothelial cells 18.3.2 Fibrosis 18.3.3 Functioning of mitochondria 18.3.3.1 Mitochondrial biosynthesis 18.3.3.2 Mitophagy 18.3.3.3 Energy metabolism 18.3.4 G2/M-arrest of tubular epithelial cells 18.3.5 Epigenetics 18.3.5.1 DNA methylation 18.3.5.2 Histone-modifications 18.3.5.3 RNA m6A methylation 18.4 Summary References Volume 2 Part 4. Tubule Physiology and Pathophysiology Chapter 19. Physiology of Renal Distal Nephron and its Clinical Relevance 19.1 Introduction 19.2 Physiology and Disorders of Transport in the mTAL 19.2.1 Bartter syndrome 19.2.1.1 Pathogenesis 19.2.1.2 Clinical presentation 19.2.1.3 Treatment 19.3 Physiology and Disorders in DCT 19.3.1 Gitelman syndrome 19.3.1.1 Pathogenesis 19.3.1.2 Clinical presentation 19.3.1.3 Treatment 19.3.2 EAST/SeSAME syndrome 19.3.2.1 Pathogenesis 19.3.2.2 Clinical presentation 19.3.2.3 Treatment 19.3.3 PHA II 19.3.3.1 Pathogenesis 19.3.3.2 Clinical presentation 19.3.3.3 Treatment 19.4 Physiology and Disorders in CNT and CD 19.4.1 PHA I 19.4.1.1 Pathogenesis 19.4.1.2 Clinical presentation 19.4.1.3 Treatment 19.4.2 Liddle syndrome 19.4.2.1 Pathogenesis 19.4.2.2 Clinical presentation 19.4.2.3 Treatment References Chapter 20. Renal Handling of Potassium and Potassium Disturbances 20.1 Introduction 20.2 Potassium Homeostasis 20.3 Renal Handling of Potassium 20.3.1 The secretion of K+ is coupled with the reabsorption of Na+ by ENaC 20.3.2 Mutations of ENaC gene 20.3.2.1 Gain-of-function mutation of ENaC gene 20.3.2.2 Loss-of-function mutation of ENaC gene 20.3.3 Regulation of ENaC expression 20.3.3.1 Mutations of MR gene 20.3.3.1.1 Gain-of-function mutations of MR gene 20.3.3.1.2 Loss-of-function mutations of MR gene 20.3.3.2 ALD levels 20.3.3.2.1 Increased ALD levels 20.3.3.2.2 Decreased ALD levels 20.3.3.3 Non-aldosterone MR agonists 20.3.3.3.1 Increased deoxycorticosterone level 20.3.3.3.2 Increased cortisol level 20.3.4 Regulation of ENaC function 20.3.4.1 Distal delivery of Na+ and water 20.3.4.1.1 Reduced Na+/water reabsorption in TAL of Henle’s loop 20.3.4.1.2 Reduced Na+/water reabsorption in DCT 20.3.4.1.3 Increased Na+/water reabsorption in DCT 20.3.5 Distal delivery of non-chloride anions 20.3.5.1 Reduced HCO−3 reabsorption in the proximal tubule 20.3.5.2 Non-chloride anions exceeding the reabsorption capacity of renal tubule 20.3.6 Impaired H+ secretion by α intercalated cells in collecting duct 20.4 Diagnostic Approach of Potassium Disorder 20.5 Summary References Chapter 21. Clinical Practice and Evaluation of the Treatment of Abnormal Phosphorus Homeostasis 21.1 Introduction 21.2 Mechanisms byWhich Phosphorus Homeostasis Is Regulated 21.2.1 NPT 21.2.2 PTH 21.2.3 FGF23 and Klotho 21.2.4 Vitamin D 21.3 Abnormal Phosphorus Homeostasis 21.3.1 Hypophosphatemia 21.3.1.1 Fanconi’s syndrome 21.3.1.2 X-linked hypophosphatemia (XLH) 21.3.1.3 Other hereditary diseases 21.3.1.4 Decreased intestinal phosphorus absorption 21.3.2 Hyperphosphatemia 21.4 Clinical Evaluation and Treatment of Hyperphosphatemia in CKD 21.4.1 Consequences of hyperphosphatemia 21.4.1.1 SHPT 21.4.1.2 Cardiovascular calcification 21.4.1.3 Bone metabolism 21.4.2 Treatment of hyperphosphatemia in CKD 21.4.2.1 Phosphorus restricted diet 21.4.2.2 Use of phosphorus binder 21.4.2.2.1 Phosphorus binder with calcium 21.4.2.2.2 Phosphorus binder without calcium 21.4.2.2.3 Phosphorus binder containing aluminum 21.4.2.3 Adequate dialysis References Chapter 22. The Story Behind the Systemic Effects of CKD Acidosis 22.1 Introduction 22.2 Definition and Diagnosis of Metabolic Acidosis in CKD Patients 22.3 Metabolic Acidosis of CKD: Expanded Concept 22.4 Renal Regulation of Acid–Base Balance 22.4.1 Ammonia metabolism 22.4.2 Titratable acids 22.4.3 Reabsorption of bicarbonate 22.4.4 Mechanisms of acidosis in CKD 22.5 Effects of CKD Acidosis on the System 22.5.1 Kidneys 22.5.1.1 Angiotensin II 22.5.1.2 ET-1 22.5.1.3 Ammonia formation 22.5.1.4 Oxidative stress 22.5.2 Bone 22.5.3 Muscle 22.5.4 Insulin resistance 22.5.5 Deposition of amyloid 22.5.6 Cardiovascular system 22.5.7 Inflammatory factors 22.5.8 Increase in mortality 22.6 Treatment of Acidosis in CKD 22.7 Summary and Prospect References Chapter 23. Nuclear Receptors in Health and Kidney Disorders: New Perspectives 23.1 Brief Introduction of Nuclear Receptors 23.2 Peroxisome Proliferator-Activated Receptors 23.2.1 PPARα 23.2.2 PPARβ/δ 23.2.3 PPARγ 23.3 Mineralocorticoid Receptor 23.4 Vitamin D Receptor 23.5 Other NRs 23.5.1 Farnesoid X receptor 23.5.2 Pregnane X receptor 23.5.3 Liver X receptors (LXRs) 23.6 Clinical Application of NR Ligands 23.7 Future Perspectives References Part 5. Renal Fibrosis: Mechanisms and Therapies Chapter 24. Renal Fibrosis: Molecular Mechanism and Signal Pathways 24.1 Introduction 24.2 Role of TGF-β/Smad in Renal Fibrosis 24.2.1 Canonical and non-canonical TGF-β signaling 24.2.2 Role of TGF-β signaling in renal fibrosis 24.3 Role ofWnt/β-catenin in Kidney Fibrosis 24.3.1 Wnt and tubular injury 24.3.2 Wnt and fibroblast activation 24.3.3 Wnt and renal inflammation 24.3.4 Wnt and podocyte injury 24.4 Role of RAS in Kidney Fibrosis 24.5 Role of Hedgehog and Notch Signaling in Kidney Fibrosis 24.6 Inflammation and Kidney Fibrosis 24.6.1 Bone marrow-derived inflammatory cells in renal fibrosis 24.6.2 Intrinsic kidney cells in renal inflammation and fibrosis 24.6.3 Proinflammatory signaling involved in renal fibrosis 24.7 Cellular Senescence and Kidney Fibrosis 24.8 The Fibrogenic Niche and Kidney Fibrosis 24.8.1 ECM components of the fibrogenic niche 24.8.2 Role of the fibrogenic niche in renal fibrosis 24.9 Role of EVs in Renal Fibrosis 24.10 Conclusion Remarks References Chapter 25. How Tubule Injury Instigates the Tubulointerstitial Inflammation and Fibrosis 25.1 Introduction 25.2 Tubulointerstitial Damage Determines the Outcome of Kidney Disease 25.3 Injury and Repair Processes of Tubular Cells 25.3.1 Cell cycle arrest 25.3.2 Mitochondria dysfunction 25.3.3 Hypoxia induced tubule damage 25.3.4 Autophagy 25.3.5 New understanding of TECs injury and repair from single-cell RNA seq 25.4 Injured Tubular cells Instigate Tubulointerstitial Inflammation and Fibrosis 25.4.1 Intercellular communication of tubules 25.4.2 Tubule-immune cell crosstalk 25.4.3 Tubule-fibroblast communication 25.4.4 Tubule-peritubular capillary crosstalk 25.5 Conclusion Acknowledgments References Chapter 26. Extracellular Vesicles: The New Player in Renal Fibrosis 26.1 Introduction 26.2 Classification and Generation of EVs 26.2.1 Exosomes 26.2.2 Microvesicles 26.2.3 EV generation in the kidney 26.3 EVs as Vicious Signalosomes in Renal Fibrosis 26.3.1 Tubule-interstitium communication 26.3.2 Intra-nephron communication 26.3.3 Inter-organ communication 26.4 EVs as Biomarkers for Renal Fibrosis 26.4.1 Urinary EV proteome 26.4.2 Urinary EV transcriptome 26.5 EVs as Nanotherapeutics for Renal Fibrosis 26.5.1 Native EVs against renal fibrosis 26.5.2 Bioengineered EVs against renal fibrosis 26.6 Conclusion Acknowledgments References Chapter 27. Role of Renin Angiotensin System in Renal Fibrosis: New Perspectives 27.1 Introduction 27.2 Renin-angiotensin System (RAS) and Its Update 27.2.1 Classical concept of RAS 27.2.2 The update in RAS profile 27.2.2.1 Revealing of ACE2-Ang1-7-Mas receptor axis 27.2.2.2 Identification of prorenin/renin receptor 27.3 The Effects of Classical RAS in Renal Fibrosis 27.3.1 Classical RAS and renal tubular epithelial cells 27.3.2 Classical RAS and renal interstitial fibroblast 27.3.3 Classical RAS and podocyte 27.3.4 Classical RAS and glomerular mesangial cell 27.4 ACE2-Ang1-7-Mas Receptor Axis and Renal Fibrosis 27.5 PRR in Renal Fibrosis 27.6 ALD in Renal Fibrosis References Chapter 28. Endothelin and Renal Disease 28.1 Introduction 28.2 Overview of ET 28.3 ET is Involved in the Regulation of Renal Function 28.3.1 Relationship between ET-1 and glomerular filtration barrier 28.3.2 ET-1 and mesangial cells 28.3.3 ET-1 and tubular epithelial cell, water, and electrolyte transport 28.3.4 ET and renal acidification 28.3.5 ET and renal vessels 28.4 ET System and Renal Disease 28.4.1 ET and chronic kidney disease 28.4.2 ET and diabetic nephropathy 28.4.3 ET and hypertensive nephropathy 28.4.4 ET and polycystic kidney disease 28.4.5 ET and focal segmental glomerulosclerosis 28.4.6 ET and other kidney diseases 28.5 Application of ET Receptor Antagonist in Renal Diseases 28.5.1 Effect of ET receptor antagonists in DN 28.5.2 Role of ET receptor antagonists in chronic kidney disease 28.5.3 Focal segmental glomerulosclerosis and ET receptor antagonists 28.6 Summary and Prospect References Chapter 29. How Mitochondria Dysfunction Affects Kidney Disease 29.1 Introduction 29.2 Mitochondrial Structural Integrity and Renal Diseases 29.2.1 Mitochondrial membrane integrity 29.2.2 mtDNA stability 29.3 Mitochondrial Function and Kidney Diseases 29.3.1 Mitochondrial bioenergetics 29.3.2 Oxidative stress 29.4 Regulation of Mitochondrial Homeostasis and Kidney Diseases 29.4.1 Mitochondrial biogenesis 29.4.2 Mitochondrial dynamics 29.4.3 Mitophagy and its contribution to pathogenesis of kidney diseases 29.5 Conclusion References Part 6. New Techniques for Diagnosing Kidney Disease (Genetics in Kidney Disease) Chapter 30. Strategy for Molecular Diagnosis of Kidney Disease 30.1 Overview of the Inherited Kidney Diseas 30.2 Molecular Diagnostic Approaches Used in IKDs 30.3 Value of Establishing a Molecular Diagnosis in Kidney Diseases 30.4 Strategy for Molecular Diagnosis of Kidney Disease 30.4.1 CAKUT 30.4.2 Steroid-resistant nephrotic syndrome 30.4.3 Alport syndrome 30.4.4 Inherited tubulopathies 30.4.5 Renal ciliopathies 30.4.6 ADTKD 30.4.7 CKD of unknown etiology 30.5 Conclusion References Chapter 31. Advances in the Treatment of Nephrotic Syndrome in Children 31.1 Introduction 31.2 Classification of PNS in Children 31.2.1 Classification 31.2.2 New classification 31.3 Advances in Immunosuppressive Therapy for SSNS 31.3.1 Glucocorticoid therapy 31.3.2 Other immunosuppressive medications 31.4 Advances in the Treatment of SRNS 31.4.1 CNIs 31.4.2 Other immunosuppressive medications 31.4.3 Others 31.5 Additional Measures for Children with PNS 31.5.1 Control edema 31.5.2 Control high blood pressure 31.5.3 Control of proteinuria 31.5.4 Prevention of infection 31.5.5 Prevention of thrombosis 31.5.6 Others References Chapter 32. Progress of Genetic Renal Diseases in Children 32.1 Introduction 32.2 Genetic NS 32.2.1 Genetic mechanisms underlying NS 32.2.2 SRNS caused by mutations in the COQ8B gene 32.2.3 Genetic diagnosis of hereditary NS 32.2.4 Genetic counseling for children with genetic NS 32.3 Renal Tubular Diseases 32.3.1 Renal tubular acidosis 32.3.2 Dent disease 32.4 Hereditary Hypophosphatemic Rickets with Hypercalciuria 32.5 Congenital Anomalies of the Kidney and Urinary Tract 32.5.1 Research progress on the genetic etiology of CAKUT 32.5.2 Copy number variations and CAKUT 32.5.3 Genetic counseling for patients with CAKUT 32.6 NPHP 32.6.1 Genetic mechanisms underlying NPHP 32.6.2 Progress and perspectives in the treatment of cystic nephropathy 32.6.3 Genetic counseling for patients with NPHP 32.7 PH 32.7.1 Genetic mechanism underlying PH1 32.7.2 Progress in the treatment of PH1 32.7.3 Management of PH1 patients with CKD and new strategies for kidney transplantation 32.7.4 Genetic counseling for patients with PH 32.8 Fabry Disease 32.8.1 Genetic mechanism underlying FD 32.8.2 Studies on FD biomarkers 32.8.3 Current status and challenges in the treatment of FD 32.8.4 FD screening and treatment practices in China 32.8.5 Genetic counseling for patients with FD References Chapter 33. Uromodulin Associated Kidney Disease: An Update Introduction 33.1 Discovery of UMOD 33.2 The Structure of UMOD 33.3 The Secretion of UMOD 33.4 Functions of UMOD 33.4.1 Protection against kidney stone 33.4.2 Protection against urinary tract infections 33.4.3 Regulates transport and blood pressure 33.4.4 Regulation of innate immunity 33.5 UMOD-Related Kidney Disease 33.5.1 ADTKD-UMOD 33.5.2 UMOD and CKD 33.5.3 UMOD and diabetic kidney disease 33.5.4 UMOD and AKI References Chapter 34. Copper Homeostasis and Renal Fibrosis 34.1 Introduction 34.2 Maintaining Copper Ion Homeostasis in the Human Body 34.2.1 Copper ion absorption and transport 34.2.2 Copper ion deficiency 34.2.3 Copper ion toxicity 34.3 Copper and Renal Fibrosis 34.3.1 Copper and excessive collagen crosslinking 34.3.2 Copper and renal tubular mitochondrial damage 34.3.3 Copper and the inflammatory response 34.3.4 Cuproptosis 34.4 Outlook References Chapter 35. Histone Acetylation and its Clinical Implications in Chronic Kidney Disease 35.1 Introduction 35.2 Histone Acetylation in Obstructive Nephropathy 35.2.1 Histone acetylation status in obstructive nephropathy 35.2.2 HATs in obstructive nephropathy 35.2.3 HDACs in obstructive nephropathy 35.3 Histone Acetylation in DN 35.3.1 Histone acetylation status in DN 35.3.2 HATs in DN 35.3.3 HDACs in DN 35.4 Histone Acetylation in Hypertensive Nephropathy 35.4.1 HAT in HTN 35.4.2 HDACs in HTN 35.5 Histone Acetylation in ADPKD 35.6 Histone Acetylation in Lupus Nephritis 35.7 Histone Acetylation in Other Kidney Diseases 35.8 Conclusion and Perspectives References Chapter 36. New Progress in the Clinical Application of Natriuretic Peptide (Hormone) 36.1 ANP Receptors and Downstream Signaling 36.2 Effect of ANP on the Kidney 36.3 Other Effects of ANP 36.3.1 Effects on fat metabolism 36.3.2 NP system and heart failure 36.4 NP Resistance: Renal Resistance andWhy Sacubitril/Valsartan Can Correct It 36.5 Role of NPs in Renal Disease References Index Comprehensive Frontier of Kidney Disease (in 2 Volumes) (Dec 17, 2024)_(9811286035)_(World Scientific Publishing Company)