Textbook of Nephro-Endocrinology

 
 
Elsevier (Verlag)
  • 2. Auflage
  • |
  • erschienen am 15. Dezember 2017
  • |
  • 584 Seiten
 
E-Book | ePUB mit Adobe-DRM | Systemvoraussetzungen
978-0-12-803248-0 (ISBN)
 

Textbook of Nephro-Endocrinology, Second Edition, continues to be the definitive translational reference in the field of nephro-endocrinology, investigating both the endocrine functions of the kidneys and how the kidney acts as a target for hormones from other organ systems. It offers researchers and clinicians expert analyses of nephro-endocrine research and translation into the treatment of diseases such as anemia, chronic kidney disease (CKD), rickets, osteoporosis, and hypoparathyroidism.

Changes to this edition include new chapters focused on hypercalcemia/hypocalcemia and the interaction of dialysis, chronic renal disease, and endocrine diseases. All chapters have been updated to include more preclinical data and more tables and schema that help translate this data into clinical recommendations. The section on hormones and renal insufficiency discusses insulin/diabetes, growth hormone, sex steroids, thyroid hormone, acid-base disturbances, and pregnancy.

  • Presents a uniquely comprehensive and cross-disciplinary look at all aspects of nephro-endocrine disorders in one reference
  • Investigates both the endocrine functions of the kidneys and how the kidney acts as a target for hormones from other organ systems
  • Offers clear translational presentations by the top endocrinologists and nephrologists in each specific hormone or functional/systems field
  • Features new and updated chapters that include more tables and schema to help translate preclinical data into clinical recommendations
  • Englisch
  • Saint Louis
  • |
  • USA
  • 85,97 MB
978-0-12-803248-0 (9780128032480)
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  • Front Cover
  • TEXTBOOK OF NEPHRO-ENDOCRINOLOGY
  • TEXTBOOK OF NEPHRO-ENDOCRINOLOGY
  • Copyright
  • Contents
  • List of Contributors
  • Preface
  • 1 - Physiology and Regulation of the Renin-Angiotensin-Aldosterone System
  • 1. THE CLASSICAL CIRCULATING RENIN-ANGIOTENSIN SYSTEM
  • 2. RENIN BIOSYNTHESIS AND SECRETION
  • 3. THE (PRO)RENIN RECEPTOR
  • 4. ANGIOTENSIN-CONVERTING ENZYME
  • 5. THE ACE-2/ANGIOTENSIN (1-7)/MAS RECEPTOR PATHWAY
  • 6. AT1 RECEPTORS
  • 7. AT2 RECEPTORS
  • 8. NEWLY DISCOVERED COMPONENTS AND ACTIONS OF THE RENIN-ANGIOTENSIN SYSTEM
  • 9. ANGIOTENSIN RECEPTOR HETERODIMERIZATION
  • 10. TISSUE RENIN-ANGIOTENSIN SYSTEMS
  • 11. INTRARENAL RENIN-ANGIOTENSIN SYSTEM
  • 12. BRAIN RENIN-ANGIOTENSIN SYSTEM
  • 13. VASCULAR TISSUE RENIN-ANGIOTENSIN SYSTEM
  • 14. CARDIAC RENIN-ANGIOTENSIN SYSTEM
  • 15. SUBCELLULAR RENIN-ANGIOTENSIN SYSTEMS
  • 16. Aldosterone and Mineralocorticoid Receptors (See Chapters 24139705914026, 28 for Additional Details)
  • 17. CLINICAL EFFECTS OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
  • 18. SUMMARY
  • References
  • 2 - The Renin-Angiotensin-Aldosterone System and the Kidney
  • 1. INTRODUCTION
  • 2. HISTORICAL BACKGROUND
  • 3. OVERVIEW OF THE RENIN-ANGIOTENSIN SYSTEM PATHWAY
  • 4. PHYSIOLOGIC EFFECTS OF RENIN-ANGIOTENSIN SYSTEM
  • 4.1 Renin-Angiotensin System and Renal Hemodynamics
  • 4.2 Renal-Angiotensin System and Tubular Function
  • 4.2.1 Proximal Tubule
  • 4.2.2 Loop of Henle
  • 4.2.3 Distal Convoluted Tubule
  • 4.2.4 Collecting Duct
  • 5. RENIN-ANGIOTENSIN SYSTEM IN HUMAN DISEASE
  • 5.1 Renin-Angiotensin System in Chronic Renal Disease
  • 5.2 Renin-Angiotensin System and Renin-Angiotensin System Blockade in Diabetic Nephropathy
  • 5.3 Renin-Angiotensin System Blockade in Other Proteinuric Chronic Kidney Diseases
  • 5.4 Renin-Angiotensin System in Lupus and Other Autoimmune Disease
  • 5.5 Renin-Angiotensin System in Acute Renal Failure
  • 5.6 Renin-Angiotensin System in Obstructive Uropathy
  • 5.7 Renin-Angiotensin System in Congenital Abnormalities
  • 6. CONCLUSION
  • References
  • 3 - The Renin-Angiotensin System and the Heart
  • 1. INTRODUCTION
  • 2. CARDIAC RAS
  • 2.1 Update on Tissue RAS Biotransformation Processes
  • 2.2 Local Versus Endocrine Origin
  • 2.3 RAS Actions at the Cellular Level
  • 2.4 RAS and the Coronary Circulation
  • 3. SIGNIFICANCE OF THE RAS ON CARDIAC FUNCTION
  • 3.1 RAS and Cardiac Remodeling
  • 4. CONCLUSIONS
  • References
  • 4 - Renin-Angiotensin Blockade: Therapeutic Agents
  • 1. INTRODUCTION
  • 2. THERAPEUTIC CLASSES
  • 3. PHARMACOLOGY
  • 3.1 Angiotensin-Converting Enzyme Inhibitors
  • 3.1.1 Pharmacokinetics
  • 3.1.2 Tissue Binding
  • 3.1.3 Application of Pharmacologic Differences
  • 3.2 Angiotensin Receptor Blockers
  • 3.3 Pharmacokinetics
  • 3.3.1 Bioavailability
  • 3.3.2 Dose Proportionality
  • 3.3.3 Volume of Distribution
  • 3.3.4 Protein Binding
  • 3.3.5 Metabolism and Active Metabolite Generation
  • 3.3.6 Route of Elimination
  • 3.3.7 Receptor Binding and Half-Life
  • 3.3.8 Application of Pharmacologic Differences/Receptor Affinity
  • 4. CHRONOTHERAPEUTICS WITH RENIN-ANGIOTENSIN SYSTEM INHIBITORS
  • 5. DIRECT RENIN INHIBITORS
  • 5.1 Pharmacokinetics
  • 6. HEMODYNAMIC EFFECTS OF RAS INHIBITORS
  • 7. ADDITIONAL PATHWAY CONSIDERATIONS AND MECHANISM OF ACTION FOR RAS INHIBITORS
  • 8. BLOOD PRESSURE LOWERING EFFECT
  • 9. RENIN-ANGIOTENSIN SYSTEM INHIBITORS WITH OTHER AGENTS
  • 10. SIDE EFFECTS PARTICULAR TO ANGIOTENSIN-RECEPTOR BLOCKERS
  • 11. SIDE EFFECTS UNIQUE TO DIRECT RENIN INHIBITORS
  • 12. SIDE EFFECTS UNIQUE TO ACE INHIBITORS
  • 13. SELECT SIDE EFFECT COMMON TO ALL RENIN-ANGIOTENSIN SYSTEM INHIBITORS
  • References
  • Further Reading
  • 5 - Vasopressin in the Kidney-Historical Aspects
  • 1. INTRODUCTION
  • 2. HYPOTHALAMUS
  • 3. VASOPRESSIN RECEPTORS
  • 3.1 Localization of Vasopressin Receptors in the Kidney
  • 3.2 Action of Vasopressin in the Toad Bladder, Collecting Tubules, and Inner Medulla
  • 3.3 Vasopressin Effects in the Other Renal Tubules
  • 4. AQUAPORINS
  • 4.1 Acute Regulation of Aquaporin Transport by Vasopressin
  • 4.2 Long-Term Effect on Aquaporin by Vasopressin
  • 5. VASOPRESSIN-REGULATED UREA TRANSPORT
  • 5.1 Red Blood Cells
  • 5.2 Inner Medullary Collecting Duct
  • 5.3 Urea Transport Proteins
  • 5.4 Acute Regulation of Urea Transport by Vasopressin
  • 5.5 Long-Term Regulation of Urea Transport by Vasopressin
  • 6. NEPHROGENIC DIABETES INSIPIDUS
  • 7. VAPTANS
  • 8. SUMMARY
  • References
  • 6 - Molecular Biology and Gene Regulation
  • 1. INTRODUCTION
  • 2. AVP SYNTHESIS, STORAGE, AND RELEASE
  • 2.1 Structure, Synthesis, and Secretion
  • 2.2 Half-Life and Clearance
  • 2.3 Similarity to Oxytocin
  • 2.4 Factors Regulating Its Secretion
  • 2.5 Pathology Associated With Dysregulation of AVP Secretion
  • 3. VASOPRESSIN RECEPTORS
  • 3.1 Receptor Subclasses
  • 3.2 V1a, V1b, and V2 Cloning
  • 3.3 Tissue/Cellular Localization
  • 3.4 Molecular Structure
  • 3.5 Signaling of Vasopressin Receptors
  • 3.6 Receptor Regulation and Desensitization
  • 3.7 Actions and Interactions of AVP Receptors
  • 4. CELLULAR REGULATION OF WATER, ELECTROLYTE, AND MINERAL REABSORPTION
  • 4.1 Water
  • 4.2 NaCl
  • 4.3 The CD and NaCl Uptake in Response to AVP
  • 4.4 Regulation of CD ENaC by AVP
  • 4.5 The TAL and NaCl Uptake in Response to AVP
  • 4.6 AVP Increases the Activity of NKCC2
  • 4.7 Regulation of Na-K-ATPase by AVP
  • 4.8 Potassium Conductance is Regulated by AVP
  • 4.9 AVP Increases Chloride Reabsorption in the TAL
  • 4.10 AVP Can Elicit Both Reabsorption and Secretion of Chloride in the Distal Tubule
  • 4.11 AVP and Chloride/Bicarbonate Exchange
  • 4.12 Urea Reabsorption is Stimulated by AVP
  • 4.13 Molecular Biology and UT-A1
  • 4.14 UT-A2 is Increased by AVP
  • 4.15 Regulation of Calcium and Magnesium Reabsorption by AVP
  • 4.16 Chronic Adaptations in the TAL Due to AVP
  • 5. VASOPRESSIN, RENAL HEMODYNAMICS, AND BLOOD PRESSURE
  • 5.1 AVP and Renal Blood Flow
  • 5.2 Glomerular Filtration Rate (GFR)
  • 5.3 Vasopressin and Blood Pressure Control
  • 5.4 V2 Receptors are Coupled to Nitric Oxide Generation
  • 5.5 Hypertension May Correlate With Urinary Concentrating Ability
  • References
  • 7 - Vasopressin Antagonists in Physiology and Disease
  • 1. INTRODUCTION
  • 2. PHYSIOLOGIC ANTAGONISTS
  • 2.1 Inhibition of Vasopressin Release
  • 2.2 Inhibition of Vasopressin Action
  • 3. VASOPRESSIN ANTAGONISTS AND THEIR ROLE IN THE TREATMENT OF WATER-RETAINING DISORDERS
  • 3.1 Vasopressin Antagonists in Euvolemic Hyponatremia
  • 3.1.1 Hypothyroidism
  • 3.1.2 Addison's Disease and Hypopituitarism
  • 3.1.3 Syndrome of Inappropriate Antidiuretic Hormone Secretion
  • 3.2 Vasopressin Antagonists in Hypervolemic Hyponatremia
  • 3.2.1 Cardiac Failure
  • 3.2.2 Cirrhosis
  • 3.3 Resistance to Vasopressin Antagonists
  • 4. ARE VASOPRESSIN ANTAGONISTS SAFE?
  • 5. SUMMARY AND UNANSWERED QUESTIONS
  • References
  • 8 - Diabetes Insipidus and Syndrome of Inappropriate Antidiuretic Hormone
  • 1. INTRODUCTION
  • 2. DIABETES INSIPIDUS AND SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
  • 2.1 Arginine Vasopressin and Water Homeostasis
  • 2.2 Diabetes Insipidus
  • 2.2.1 Nephrogenic Diabetes Insipidus (Table 8.1)
  • 2.2.2 Congenital Nephrogenic Diabetes Insipidus
  • 2.2.2.1 Genetics
  • 2.2.2.2 Treatment
  • 2.2.3 Acquired Nephrogenic Diabetes Insipidus
  • 2.2.3.1 Renal Disease
  • 2.2.3.2 Sickle Cell Disease
  • 2.2.3.3 Lithium
  • 2.2.3.4 Hypokalemia
  • 2.2.3.5 Hypercalcemia and Hypercalciuria
  • 2.2.4 Central Diabetes Insipidus
  • 2.2.4.1 Genetic Mutations
  • 2.2.4.2 Congenital Malformations
  • 2.2.4.3 Acquired Central Diabetes Insipidus
  • 2.2.4.4 Idiopathic Central Diabetes Insipidus and Autoimmunity
  • 2.2.4.5 Granulomatous Diseases
  • 2.2.4.6 Neoplasms
  • 2.2.4.7 Traumatic Brain Injury
  • 2.2.4.8 Postsurgical
  • 2.2.5 MRI in the Diagnosis Central Diabetes Insipidus
  • 2.2.6 Diagnosis of Diabetes Insipidus
  • 2.2.7 Treatment of Central Diabetes Insipidus
  • 2.2.8 Treatment of Hypernatremia Due to Diabetes Insipidus
  • 2.2.8.1 Case 1 Nephrogenic Diabetes Insipidus65
  • 2.2.8.2 Case 2 Central Diabetes Insipidus
  • 2.3 Syndrome of Inappropriate Antidiuretic Hormone Secretion
  • 2.3.1 Pathogenesis of Hyponatremia
  • 2.3.2 Pathogenesis of Syndrome of Inappropriate Antidiuretic Hormone
  • 2.3.3 Arginine Vasopressin Regulation in Syndrome of Inappropriate Antidiuretic Hormone (Fig. 8.4)
  • 2.3.4 Nephrogenic Syndrome of Inappropriate Antidiuresis
  • 2.3.5 Epidemiology of Syndrome of Inappropriate Antidiuretic Hormone
  • 2.3.6 Exercise-Associated Hyponatremia
  • 2.3.7 "Ecstasy" (3,4-Methylenediaxymethamphetamine)
  • 2.3.8 HIV
  • 2.3.9 Medications
  • 2.3.10 dDAVP and Oxytocin
  • 2.3.11 Cerebral Salt Wasting
  • 2.3.12 Diagnosis of Syndrome of Inappropriate Antidiuretic Hormone and Evaluation of Hyponatremia
  • 2.3.13 Treatment of Syndrome of Inappropriate Antidiuretic Hormone
  • 3. HYPONATREMIC ENCEPHALOPATHY
  • 3.1 Cerebral Edema and Brain Cell Volume Regulation
  • 3.2 Clinical Symptoms
  • 3.3 Neurogenic Pulmonary Edema
  • 3.4 Risk Factors for Developing Hyponatremic Encephalopathy (Table 8.7)
  • 3.4.1 Age
  • 3.4.2 Gender
  • 3.4.3 Hypoxia
  • 3.5 0.9% NaCl as Prophylaxis Against Hyponatremia
  • 3.6 Treatment of Hyponatremic Encephalopathy
  • 3.7 Cerebral Demyelination in the Correction of Hyponatremia
  • References
  • 9 - The Cardiac Natriuretic Peptide System: Linking the Heart and Kidney in Cardiorenal Homeostasis and Therapeutics
  • 1. NATRIURETIC PEPTIDES
  • 2. NATRIURETIC PEPTIDE THERAPEUTICS
  • 3. DESIGNER NATRIURETIC PEPTIDES FOR CARDIORENAL DISEASE
  • 4. NEPRILYSIN AND NEPRILYSIN INHIBITION
  • 5. NEPRILYSIN INHIBITION AS A THERAPEUTIC STRATEGY FOR TARGETING THE CARDIORENAL AXIS
  • 6. FUTURE DIRECTIONS
  • Acknowledgments
  • References
  • 10 - Aldosterone's Mechanism of Action: Genomic and Nongenomic Signaling
  • 1. INTRODUCTION
  • 2. THE MINERALOCORTICOID RECEPTOR
  • 2.1 Nuclear Mineralocorticoid Receptor and Cytosolic Mineralocorticoid Receptor
  • 2.2 Cell Membrane Mineralocorticoid Receptor
  • 2.3 Coregulators of Aldosterone Signaling
  • 2.4 Mineralocorticoid Receptor Interaction With the Estrogen Receptor
  • 2.5 Mineralocorticoid Receptor Ligands and Their Selectivity
  • 3. GENOMIC ACTIONS OF ALDOSTERONE
  • 3.1 Classical Target Tissues
  • 3.2 Nonclassical Target Tissues
  • 3.2.1 Cardiac Tissue
  • 3.2.2 Endothelium
  • 3.2.3 Vascular Smooth Muscle Cells
  • 3.2.4 Adipose Tissue
  • 4. NONGENOMIC ACTIONS OF ALDOSTERONE
  • 4.1 Rapid Signaling Cascades
  • 4.2 Striatin
  • 4.3 G Protein-Coupled Estrogen Receptor
  • 5. EPIGENETIC EFFECTS
  • 6. MINERALOCORTICOID RECEPTOR MODULATORS
  • 6.1 Sodium
  • 6.2 Caveolin-1
  • 6.3 Rac1
  • 7. NOVEL MINERALOCORTICOID RECEPTOR?ANTAGONISTS
  • 8. CONCLUSIONS
  • References
  • 11 - Erythropoietin: An Historical Overview of Physiology, Molecular Biology, and Gene Regulation
  • 1. INTRODUCTION
  • 2. HORMONAL REGULATION OF ERYTHROPOIESIS
  • 3. IDENTIFICATION OF THE SITE OF ERYTHROPOIETIN PRODUCTION
  • 4. ASSAYS OF ERYTHROPOIETIN
  • 5. ISOLATION AND CHARACTERIZATION OF ERYTHROPOIETIN
  • 6. ERYTHROPOIETIN EFFECTOR MECHANISMS
  • 7. REGULATION OF ERYTHROPOIESIS BY HYPOXIA
  • 8. REGULATORY ELEMENTS OF ERYTHROPOIETIN GENE
  • 9. ERYTHROPOIETIN-THE PARADIGM FOR GENE REGULATION BY HYPOXIA
  • 10. HYPOXIA-INDUCIBLE FACTOR
  • 11. THE ELUSIVE NATURE OF THE OXYGEN SENSOR
  • 12. DEGRADATION OF HYPOXIA-INDUCIBLE FACTOR BY THE UBIQUITIN-PROTEOSOMAL PATHWAY
  • 13. TARGETING OF HYPOXIA-INDUCIBLE FACTOR BY THE VON HIPPEL-LINDAU E3 UBIQUITIN LIGASE
  • 14. REGULATION OF THE HYPOXIA-INDUCIBLE FACTOR-VON HIPPEL-LINDAU INTERACTION
  • 15. THE HYPOXIA-INDUCIBLE FACTOR HYDROXYLASES AS OXYGEN SENSORS
  • 16. DISRUPTION OF THE OXYGEN-SENSING PATHWAY IN CANCER
  • 17. DISRUPTION OF THE OXYGEN-SENSING PATHWAY IN HEREDITARY POLYCYTHEMIA
  • 18. PHARMACOLOGICAL MANIPULATION OF HYPOXIA-INDUCIBLE FACTOR
  • 19. SUMMARY
  • Conflict of interest statement
  • References
  • 12 - Erythropoiesis: The Roles of Erythropoietin and Iron
  • 1. ERYTHROPOIESIS: AN OVERVIEW
  • 1.1 Hematopoiesis
  • 1.2 Erythropoiesis
  • 1.2.1 Regulation of Erythropoiesis by?Hypoxia-Inducible Factors
  • 1.2.2 Growth Factors Important for Hematopoiesis and Erythropoiesis
  • 2. ROLE OF ERYTHROPOIETIN IN ERYTHROPOIESIS
  • 2.1 Erythropoietin Receptor (See Fig. 12.1)
  • 2.2 Intracellular Signaling Mediators of Erythropoietin
  • 3. ROLE OF IRON IN ERYTHROPOIESIS
  • 3.1 Hepcidin and Regulation of Serum Iron Levels
  • 3.1.1 Erythroferrone
  • 3.1.2 Growth Differentiation Factor 15
  • 3.1.3 Twisted Gastrulation Protein Homolog 1
  • 3.2 Iron and Regulation of Hemoglobin Production
  • 3.3 Regulation of Iron Storage
  • Acknowledgments
  • References
  • 13 - Development of Recombinant Erythropoietin and Erythropoietin Analogs
  • 1. INTRODUCTION
  • 2. HISTORY OF RECOMBINANT HUMAN ERYTHROPOIETIN
  • 3. BIOSIMILAR ERYTHROPOIETINS
  • 4. POTENTIAL STRATEGIES FOR MODIFYING ERYTHROPOIETIN TO CREATE NEW ERYTHROPOIETIN ANALOGS
  • 5. DARBEPOETIN ALFA
  • 5.1 Intravenous Administration-Hemodialysis Patients
  • 5.2 Subcutaneous Administration-Hemodialysis Patients
  • 5.3 Subcutaneous Administration-Predialysis Chronic Kidney Disease Patients
  • 6. CONTINUOUS ERYTHROPOIETIN RECEPTOR ACTIVATOR
  • 6.1 Effects of CERA In Vitro and in Animal Models
  • 6.2 Continuous Erythropoietin Receptor Activator in Healthy Subjects
  • 6.3 Effects of Continuous Erythropoietin Receptor Activator in Patients With Chronic Kidney Disease Anemia
  • 6.4 Safety and Tolerability of Continuous Erythropoietin Receptor Activator
  • 7. SMALL MOLECULE ERYTHROPOIESIS-STIMULATING AGENTS
  • 7.1 Peptide-Based Erythropoiesis-Stimulating Agents
  • 7.2 Nonpeptide-Based Erythropoiesis-Stimulating Agents
  • 8. OTHER STRATEGIES FOR STIMULATING ERYTHROPOIESIS
  • 9. CONCLUSIONS
  • References
  • Further Reading
  • 14 - Insulin Resistance and the Metabolic Syndrome in Chronic Renal Disease
  • 1. INTRODUCTION
  • 2. HISTORICAL PERSPECTIVE
  • 3. CELLULAR MECHANISMS OF INSULIN SECRETION AND ACTION
  • 4. CLINICAL PHYSIOLOGY OF INSULIN RESISTANCE
  • 5. MEASUREMENT OF INSULIN RESISTANCE
  • 6. METABOLIC SYNDROME
  • 6.1 Overview
  • 6.2 Definition
  • 6.3 Obesity
  • 6.4 Hyperglycemia
  • 6.5 Hypertension
  • 6.6 Dyslipidemia
  • 6.7 Proteinuria
  • 6.8 Hyperuricemia and Nephrolithiasis
  • 7. PATHOGENESIS OF INSULIN RESISTANCE IN CHRONIC KIDNEY DISEASE
  • 8. REGULATION OF RENAL GLUCOSE PRODUCTION
  • 9. SYNDROMES OF SEVERE INSULIN RESISTANCE
  • 10. TREATMENT
  • 10.1 Dietary Management
  • 10.2 Exercise
  • 10.3 Insulin Sensitizers
  • 11. MANAGEMENT OF DIABETES IN CHRONIC KIDNEY DISEASE
  • 12. HYPERGLYCEMIA ASSOCIATED WITH RENAL TRANSPLANTATION
  • 13. CONCLUSIONS
  • References
  • 15 - Growth Hormone
  • 1. GROWTH HORMONE AND INSULIN-LIKE GROWTH FACTOR-1 IN RENAL FAILURE
  • 1.1 Disturbance of the Normal GH/IGF-1 Axis
  • 1.1.1 Introduction
  • 1.1.2 Normal GH/IGF-1 Axis
  • 1.1.3 Pathophysiology of the Disordered GH/IGF-1 Axis in Renal Insufficiency
  • 1.1.4 Growth Hormone and Growth Hormone Resistance in CKD
  • 1.1.5 Insulin-Like Growth Factor-1 and?Insulin-Like Growth Factor-1 Abnormalities in CKD
  • 2. PEDIATRIC IMPLICATIONS: GROWTH FAILURE AND THE GH/IGF-1 AXIS IN CKD
  • 2.1 Impact of Growth Failure in Children With CKD
  • 2.2 Disordered Growth in Children With Renal Failure: Etiology of Growth Impairment
  • 2.2.1 Nonmodifiable Factors
  • 2.2.2 Modifiable Factors
  • 3. ADULT IMPLICATIONS: MYRIAD EFFECTS OF DISTURBED GH/IGF-1 AXIS IN CKD
  • 4. EFFECTS OF RECOMBINANT GROWTH HORMONE TREATMENT IN RENAL FAILURE
  • 4.1 Growth and the Pediatric Response to GH Therapy
  • 4.2 Safety of GH Therapy
  • 4.3 Dosing Recommendations
  • 4.4 Effects in Adults With Chronic Renal Failure Treated With GH
  • 4.5 Effects in Adults With Acute Renal Failure Treated With rGH
  • 4.6 Effects of Recombinant IGF-1 Treatment in Chronic and Acute Renal Failure
  • 5. THE HORIZON FOR IMPROVING GROWTH AND ANABOLISM IN RENAL FAILURE
  • 6. SUMMARY
  • References
  • 16 - Sexual Dysfunction in Men and Women With Chronic Kidney Disease
  • 1. INTRODUCTION
  • 2. SEXUAL DYSFUNCTION IN UREMIC MEN
  • 2.1 Vascular System
  • 2.2 Neurologic System
  • 2.3 Endocrine System
  • 2.3.1 Testicular Function
  • 2.3.2 Sex Steroids
  • 2.3.3 Hypothalamic-Pituitary Function
  • 2.3.4 Prolactin Metabolism
  • 2.3.5 Gynecomastia
  • 2.4 Psychologic System
  • 3. EVALUATION OF SEXUAL DYSFUNCTION IN THE?UREMIC MAN
  • 4. TREATMENT OF SEXUAL DYSFUNCTION IN THE?UREMIC MAN
  • 5. OUTCOMES ASSOCIATED WITH HYPOGONADISM AND TREATMENT
  • 6. SEXUAL DYSFUNCTION IN UREMIC WOMEN
  • 6.1 Normal Menstrual Cycle
  • 6.2 Hormonal Disturbances in Uremic Premenopausal Women
  • 6.3 Prolactin and Galactorrhea
  • 6.4 Hormonal Disturbances in Uremic Postmenopausal Women
  • 7. TREATMENT
  • References
  • 17 - Metabolic Acidosis of Chronic Kidney Disease
  • 1. INTRODUCTION
  • 2. REGULATION OF ACID-BASE BALANCE WITH NORMAL RENAL FUNCTION AND CHRONIC KIDNEY DISEASE
  • 3. ACID-BASE PRODUCTION
  • 4. RENAL BICARBONATE GENERATION
  • 5. CELLULAR BUFFERING
  • 6. RENAL TUBULAR BICARBONATE REABSORPTION
  • 7. HORMONAL REGULATION OF ACID-BASE BALANCE WITH NORMAL RENAL FUNCTION AND CKD
  • 8. ALDOSTERONE
  • 9. ANGIOTENSIN II
  • 10. PARATHYROID HORMONE
  • 11. GLUCOCORTICOIDS
  • 12. ANTIDIURETIC HORMONE
  • 13. GLUCAGON
  • 14. ENDOTHELIN
  • 15. INSULIN
  • 16. GROWTH HORMONE AND IGF-1
  • 17. CLINICAL CHARACTERISTICS OF THE METABOLIC ACIDOSIS OF CHRONIC KIDNEY DISEASE
  • 17.1 Onset, Prevalence, and Magnitude
  • 18. SERUM ELECTROLYTE PATTERN
  • 19. RENAL TUBULAR BICARBONATE GENERATION AND URINARY ACIDIFICATION
  • 20. CLINICAL CHARACTERISTICS OF ACID-BASE PARAMETERS IN DIALYSIS PATIENTS
  • 21. EFFECTS OF METABOLIC ACIDOSIS OF CKD?ON CELLULAR FUNCTION
  • 22. EXACERBATION OR PRODUCTION OF BONE DISEASE
  • 23. MUSCLE WASTING
  • 24. REDUCED ALBUMIN SYNTHESIS
  • 25. ACCELERATION OF PROGRESSION OF CKD
  • 26. EXACERBATION OR DEVELOPMENT OF?CARDIAC DISEASE
  • 27. IMPAIRED GLUCOSE HOMEOSTASIS AND?LIPID METABOLISM
  • 28. LEPTIN
  • 29. ACCUMULATION OF ?2-MICROGLOBULIN
  • 30. GROWTH HORMONE AND THYROID FUNCTION
  • 31. INFLAMMATORY RESPONSE
  • 32. TREATMENT OF THE METABOLIC ACIDOSIS OF CKD
  • References
  • 18 - Pregnancy and the Kidney
  • 1. NORMAL PREGNANCY
  • 1.1 Renal Adaptation
  • 1.2 Cardiac and Vascular Adaptation in Pregnancy
  • 2. PREECLAMPSIA AND HELLP SYNDROME
  • 2.1 Epidemiology and Risk Factors
  • 2.2 Clinical Features and Pathophysiology
  • 2.2.1 Hypertension
  • 2.2.2 Proteinuria
  • 2.2.3 Uric Acid
  • 2.2.4 Renal Changes and Pathology
  • 2.2.5 Severe Preeclampsia and Eclampsia
  • 2.2.6 HELLP Syndrome and Hematological Abnormalities
  • 2.3 Long-Term Cardiovascular and Renal Outcomes
  • 2.4 Pathogenesis of Preeclampsia (See Fig. 18.2)
  • 2.4.1 Abnormal Placentation
  • 2.4.2 Placental Vascular Development
  • 2.4.3 Maternal Endothelial Function
  • 2.4.4 Immunologic Maladaptation
  • 2.4.5 Oxidative Stress
  • 2.4.6 Angiogenic Factors
  • 2.4.7 Renin-Angiotensin System
  • 2.5 Screening and Treatment
  • 2.5.1 Screening
  • 2.5.2 Management and Treatment
  • 2.5.3 Management of the HELLP Syndrome
  • 3. OTHER HYPERTENSIVE DISORDERS OF PREGNANCY
  • 3.1 Chronic Hypertension
  • 3.2 Gestational Hypertension
  • 3.3 Secondary Causes of Hypertension in Pregnancy
  • 3.4 Management of Chronic Hypertension in Pregnancy
  • 4. RENAL FAILURE IN PREGNANCY
  • 4.1 Acute Renal Failure
  • 4.1.1 Acute Kidney Injury
  • 4.1.2 Cortical Necrosis
  • 4.1.3 Thrombotic Microangiopathy
  • 4.1.4 Obstruction
  • 4.2 Chronic Kidney Disease
  • 4.2.1 Diabetic Nephropathy
  • 4.2.2 Lupus Nephritis
  • 4.3 End-Stage Renal Disease and Dialysis
  • 4.4 Renal Transplant in Pregnancy
  • 4.4.1 Maternal, Fetal, and Graft Outcomes
  • 4.4.2 Immunosuppressive Therapy
  • 4.4.3 Acute Rejection
  • References
  • 19 - Vitamin D: Molecular Biology and Gene Regulation
  • 1. VITAMIN D
  • 2. THE 1,25-DIHYDROXYVITAMIN D/VITAMIN D RECEPTOR COMPLEX
  • 2.1 Gene Targets and Biological Actions
  • 2.2 Structure Function
  • 2.3 Regulation of Gene Expression
  • 2.3.1 Ligand/Vitamin D Receptor Complex Formation
  • 2.3.2 Vitamin D Receptor Heterodimerization With Retinoid X Receptor
  • 2.3.3 DNA Binding
  • 2.3.4 Gene Transactivation/Transrepression
  • 2.3.4.1 Transactivation
  • 2.3.4.2 Transrepression
  • 2.3.5 Nongenomic Actions of Calcitriol
  • 2.3.6 Vitamin D Receptor Polymorphisms
  • 2.3.7 Control of mRNA Translation
  • 3. RELEVANCE OF 1,25-DIHYDROXYVITAMIN D/VITAMIN D RECEPTOR ACTIONS IN HEALTH AND IN KIDNEY DISEASE
  • 3.1 Intestine
  • 3.2 Parathyroid Glands
  • 3.3 Bone
  • 3.4 Kidney
  • 3.5 Cardiovascular System
  • 4. CONCLUDING REMARKS
  • Acknowledgments
  • References
  • 20 - Clinical Syndromes of Vitamin D and Phosphate Dysregulation
  • 1. INTRODUCTION
  • 2. METABOLISM
  • 2.1 The Role of Cytochromes
  • 3. TRANSPORT
  • 4. MECHANISM OF ACTION
  • 5. FUNCTIONS OF VITAMIN D
  • 6. RECOMMENDED DIETARY ALLOWANCE GUIDELINES FOR VITAMIN D
  • 7. VITAMIN D DYSREGULATION: EPIDEMIOLOGY OF INSUFFICIENCY AND TOXICITY STATES
  • 8. SKELETAL MANIFESTATIONS OF VITAMIN D DYSREGULATION
  • 8.1 Rickets
  • 8.2 Osteomalacia
  • 9. LOOKING BEYOND THE BONES: EXTRASKELETAL MANIFESTATIONS OF VITAMIN D DYSREGULATION
  • 9.1 Role of Vitamin D in Muscle Health
  • 9.2 Falls, Frailty, and Fractures
  • 9.3 Vitamin D and the Immune System
  • 9.4 Vitamin D and Cancer
  • 9.5 Vitamin D and Cardiovascular Diseases
  • 9.6 Chronic Kidney Disease-Related Mineral Bone Disorders and Role of Vitamin D
  • 10. VITAMIN D TOXICITY
  • 11. CONCLUSION
  • References
  • 21 - Molecular Biology of Renin and Regulation of Its Gene
  • 1. INTRODUCTION
  • 2. PRODUCTION AND ACTIVATION OF RENIN
  • 2.1 Tissue Origin of Active Renin
  • 2.2 Physiological Control of Renin Levels
  • 2.3 Ontogeny and Plasticity of Renin Expression
  • 2.4 Mechanisms of Proteolytic and Nonproteolytic Activation
  • 3. RENIN GENE STRUCTURE AND REGULATION
  • 3.1 Genomic Structure in Humans and Laboratory Animals
  • 3.2 Promoters and Enhancers in the Renin Gene
  • 4. RENIN GENE MUTATION AND DISEASE
  • 4.1 Renin Gene Polymorphisms and Hypertension
  • 4.2 Inactivation of the Renin Gene in Mouse
  • 4.3 Inactivation of the Renin Gene in Humans
  • 4.4 Potential Role of microRNAs in Regulating Renin Expression
  • 5. FUTURE PERSPECTIVES
  • Acknowledgments
  • References
  • Further Reading
  • 22 - Vitamin D and the Kidney: Introduction and Historical Perspective
  • 1. INTRODUCTION
  • 2. VITAMIN D
  • 2.1 Etiology of Rickets
  • 2.2 Search for a Remedy for Rickets
  • 2.3 Experimental Evidence of the Role of Vitamin D in Rickets
  • 2.4 Discovery of the Structure of Vitamin D
  • 2.5 Role of Vitamin D in Calcium Regulation
  • 3. ROLE OF VITAMIN D IN KIDNEY DISEASE
  • 3.1 Chronic Kidney Disease-Mineral Bone Disease (CKD-MBD)
  • 3.2 Observational Studies
  • 3.3 Randomized Controlled Trials of Nutritional Vitamin D
  • 3.4 Randomized Controlled Trials of Active Vitamin D
  • 4. ROLE OF VITAMIN D IN OTHER DISEASE STATES
  • References
  • 23 - Extrahematopoietic Actions of Erythropoietin
  • 1. THE BIOLOGY OF ERYTHROPOIETIN
  • 1.1 The Organismal Response to Cellular Stress
  • 1.1.1 The Integrated Response to Systemic Hypoxia Involves Multiple Cell Types
  • 1.1.2 The Innate Immune Response: A Balance Between Protection and Injury
  • 1.1.3 The Hypoxic Stress and Innate Immune Responses are Interrelated
  • 1.1.4 EPO Modulates Immunity
  • 1.1.5 EPO Is Essential for Normal Tissue Development and Repair
  • 1.2 Erythropoietin Structure
  • 1.3 Identity and Biology of Alternative EPO Receptors
  • 1.3.1 EPOR-ßCR
  • 1.3.2 Soluble EPOR2
  • 1.4 Specific Nonerythropoietic Ligands
  • 1.5 Nonhematopoietic Signaling Pathways
  • 2. EXAMPLES OF NONERYTHROPOIETIC ACTIVITIES OF EPO IN DIFFERENT TISSUES
  • 2.1 Endothelium
  • 2.2 Central Nervous System
  • 2.3 The Retina
  • 2.4 The Kidney
  • 2.5 The Myocardium
  • 2.6 Skin
  • 2.7 Metabolic Control and Obesity
  • 2.8 Immune Cells
  • 2.9 Other Tissues
  • 2.10 Clinical Perspective
  • References
  • 24 - Regulation of Aldosterone Production
  • 1. INTRODUCTION
  • 2. ALDOSTERONE BIOSYNTHESIS
  • 3. FACTORS REGULATING ALDOSTERONE PRODUCTION
  • 3.1 The Renin-Angiotensin-Aldosterone System
  • 3.1.1 Physiology of the Renin-Angiotensin-Aldosterone System
  • 3.1.2 AngII-Regulated Intracellular Signaling Pathways
  • 3.1.3 Chronic Effects of AngII
  • 3.2 Potassium
  • 3.2.1 Effects of Potassium on Aldosterone Production
  • 3.2.2 Potassium-Regulated Intracellular Signaling Pathways
  • 3.2.3 Chronic Effects of Potassium
  • 4. ADRENOCORTICOTROPIC HORMONE
  • 4.1 Physiology of Adrenocorticotropic Hormone-Regulated Aldosterone
  • 4.2 Adrenocorticotropic Hormone-Regulated Intracellular Signaling
  • 4.3 Chronic Action of Adrenocorticotropic Hormone on Aldosterone Production
  • 4.3.1 Other Aldosterone Secretagogues
  • 4.3.2 Inhibitors of Aldosterone Biosynthesis
  • 5. DISEASES OF ALDOSTERONE PRODUCTION
  • 5.1 Genetic Defects Causing Aldosterone Deficiency
  • 5.1.1 CYP21
  • 5.1.1.1 Diagnosis
  • 5.1.1.2 Treatment
  • 5.1.2 CYP11B2
  • 5.2 Defects Causing Aldosterone Excess
  • 5.2.1 Primary Aldosteronism
  • 5.2.1.1 Pathophysiology
  • 5.2.1.2 Diagnosis
  • 5.2.1.3 Treatment
  • 5.2.1.3.1 Bilateral Primary Aldosteronism Treatment of bilateral forms of PA is based on the administration of mineralocorticoid...
  • 5.2.1.3.2 Unilateral Primary Aldosteronism Unless there is a medical contraindication, surgery is the treatment of choice for pa...
  • 5.2.1.3.3 Molecular Mechanisms Responsible for Autonomous Aldosterone Overproduction in Sporadic and Familial Primary Aldosteron...
  • 5.2.1.3.4 KCNJ5 Mutations The KCNJ5 gene is located on chromosome 11 and encodes the inward-rectifying K+ channel GIRK4, which i...
  • 5.2.1.3.5 ATP1A1 and ATP2B3 Mutations ATP1A1 is located on chromosome 1 and encodes the a-subunit of the Na+/K+ ATPase, while AT...
  • 5.2.1.3.6 CACNA1D Mutations Voltage-gated calcium channels mediate the entry of calcium ions into excitable cells and are involv...
  • 5.2.1.3.7 CACNA1H Mutations CACNA1H is located on chromosome 16 and encodes the pore-forming alpha subunit of the T-type, low vo...
  • 6. CONCLUSIONS
  • References
  • 25 - Aldosterone and Its Cardiovascular Effects
  • 1. INTRODUCTION
  • 2. ALDOSTERONE AND THE HEART
  • 2.1 Clinical Evidence Supporting a Role for Aldosterone in the Pathophysiology of Cardiac Disease
  • 2.1.1 Heart Failure
  • 2.1.2 Hypertensive Heart Disease
  • 2.1.3 Cardiovascular Disease Associated With Insulin Resistance and Diabetes
  • 2.1.4 Diastolic Dysfunction
  • 2.1.5 Primary Aldosteronism and Cardiovascular Disease
  • 2.1.6 Mineralocorticoid Receptor Antagonists, Hyperkalemia, and Renal Function
  • 2.2 Preclinical Evidence Demonstrating a Role for Aldosterone in the Pathophysiology of Cardiovascular Disease
  • 3. ALDOSTERONE AND BRAIN
  • 4. ALDOSTERONE AND RENAL DISEASE
  • 4.1 Clinical Studies Supporting a Role for Aldosterone in the Pathophysiology of Renal Disease
  • 4.2 Aldosterone and Animal Models of Diabetic and Nondiabetic Renal Injury
  • 4.2.1 Nondiabetic Animal Models
  • 4.2.2 Diabetic Animal Models
  • 5. POTENTIAL MOLECULAR PATHWAYS MEDIATING THE ADVERSE VASCULAR EFFECTS OF ALDOSTERONE (FIG. 25.1)
  • 5.1 Mineralocorticoid Receptor Interactions With Other Receptors and Signaling Pathways
  • 5.2 Aldosterone and Vasoconstriction and Vasodilation
  • 5.3 Aldosterone and Inflammation
  • 5.4 Mineralocorticoid Receptor and Adipocytes
  • 6. THERAPEUTIC CONSIDERATIONS
  • 7. CONCLUSIONS
  • References
  • 26 - Aldosterone: History and Introduction
  • 1. EARLY HISTORY OF ALDOSTERONE
  • 1.1 Early Work on Adrenal Extracts
  • 1.1.1 Activity of Amorphous Fraction
  • 1.1.2 Loss of Faith in Significance of the Amorphous Fraction
  • 1.2 Direct Electrolyte Assays
  • 1.3 Studies on Adrenal Extract Using the 24Na/42K Assay and Paper Chromatography
  • 1.4 Discovery of Electrocortin (Aldosterone) as a Hormone
  • 1.5 Crystallization of Electrocortin (Aldosterone) and Isolation in Crystalline Form
  • 1.5.1 Purification and Early Structural Studies
  • 1.5.2 Isolation in Crystalline Form
  • 1.6 Identification and Synthesis of Aldosterone (Electrocortin)
  • 1.7 Adrenal Site of Production of Steroids
  • 1.8 Metabolism and Biosynthesis of Aldosterone
  • 1.8.1 Metabolism
  • 1.8.2 Biosynthesis of Aldosterone
  • 2. ALDOSTERONE AND MINERALOCORTICOID RECEPTOR IN CLINICAL MEDICINE
  • 2.1 Congestive Heart Failure
  • 2.2 Primary Aldosteronism
  • 2.3 Resistant Hypertension and Mineralocorticoid Receptor-Associated Hypertension
  • 3. MINERALOCORTICOID RECEPTOR ANTAGONISTS
  • 3.1 Spironolactone
  • 3.2 Eplerenone
  • 3.3 Third-Generation Mineralocorticoid Receptor Antagonists
  • 3.4 Fourth-Generation Mineralocorticoid Receptor Antagonists
  • References
  • 27 - Thyroid Status in Chronic Renal Failure Patients
  • 1. EPIDEMIOLOGY OF THYROID DYSFUNCTION IN KIDNEY DISEASE
  • 2. THYROID PHYSIOLOGY
  • 3. THYROID FUNCTIONAL TEST DERANGEMENTS IN KIDNEY DISEASE
  • 3.1 Thyrotropin
  • 3.2 Triiodothyronine
  • 3.3 Reverse Triiodothyronine
  • 3.4 Thyroxine
  • 3.5 Antithyroid Peroxidase Antibodies
  • 4. POTENTIAL MECHANISMS LINKING THYROID AND KIDNEY DISEASE
  • 4.1 Thyroid Dysfunction as a Risk Factor for Altered Kidney Structure and Function
  • 4.2 Kidney Disease as a Risk Factor for Thyroid Dysfunction
  • 5. THYROID DYSFUNCTION AND OUTCOMES
  • 5.1 Thyroid Dysfunction and Cardiovascular Disease in the General Population
  • 5.2 Thyroid Dysfunction and Mortality in the General Population
  • 5.3 Thyroid Dysfunction, Cardiovascular Disease, and Mortality in Chronic Kidney Disease: Triiodothyronine and Thyroxine
  • 5.4 Thyroid Dysfunction, Cardiovascular Disease, and Mortality in Chronic Kidney Disease: Thyrotropin
  • 6. TREATMENT OF THYROID DYSFUNCTION
  • 7. FUTURE DIRECTIONS
  • References
  • 28 - Aldosterone/Mineralocorticoid Receptors and Their Renal Effects: Molecular Biology and Gene Regulation
  • 1. INTRODUCTION
  • 2. ALDOSTERONE-BINDING SITES AND THE MINERALOCORTICOID RECEPTOR
  • 3. MOLECULAR BIOLOGY OF THE MINERALOCORTICOID RECEPTOR
  • 4. GENOMIC STRUCTURE AND ORGANIZATION
  • 5. POSTTRANSLATIONAL MODIFICATIONS OF THE MINERALOCORTICOID RECEPTOR
  • 5.1 Phosporylation
  • 5.2 Sumoylation
  • 5.3 Acetylation
  • 5.4 Ubiquitylation
  • 5.5 Oxidation
  • 6. OLIGOMERIC STRUCTURE OF STEROID RECEPTORS
  • 7. CYTOPLASMIC-NUCLEAR SHUTTLING OF STEROID RECEPTORS
  • 7.1 Mineralocorticoid Receptor Trafficking
  • 8. MINERALOCORTICOID RECEPTOR SELECTIVITY
  • 9. DISTRIBUTION OF THE MINERALOCORTICOID?RECEPTOR IN THE NEPHRON
  • 10. PROTEINS INDUCED BY ALDOSTERONE IN TRANSPORT EPITHELIA
  • 11. NONGENOMIC EFFECTS OF ALDOSTERONE IN THE KIDNEY
  • 12. CROSS TALK OF THE MINERALOCORTICOID RECEPTOR WITH MEMBRANE RECEPTORS
  • 13. ALDOSTERONE EFFECTS MEDIATED BY GPER (GPR30)
  • 14. RENAL NONGENOMIC EFFECTS OF ALDOSTERONE
  • 15. PHYSIOLOGICAL AND PHARMACOLOGICAL ROLE OF ANTAGONISTS OF THE MINERALOCORTICOID?RECEPTOR IN HUMAN PHYSIOLOGY AND PATHOLOGY
  • 16. CONCLUSIONS
  • References
  • 29 - The History of the Renin-Angiotensin System
  • 1. INTRODUCTION
  • 2. THE 20TH CENTURY
  • 3. THE 21ST CENTURY
  • 3.1 The Ambiguity of the Renin-Angiotensin-Aldosterone System
  • 3.2 The Discovery of New Monogenic Forms of Hypertension
  • 4. THE DREAM TO BE NORMOTENSIVE AND DRUG FREE
  • 5. CONCLUSION
  • References
  • Further Reading
  • 30 - Molecular Biology of Parathyroid Hormone
  • 1. BIOSYNTHESIS AND METABOLISM
  • 1.1 Regulation
  • 1.2 Circulating Forms of Parathyroid Hormone
  • 1.3 Measurement
  • 2. PARATHYROID HORMONE RECEPTORS
  • 2.1 Isoforms
  • 3. MECHANISMS OF PARATHYROID HORMONE BINDING AND PARATHYROID HORMONE RECEPTOR SIGNALING
  • 3.1 Parathyroid Hormone Binding
  • 3.2 Parathyroid Hormone Receptor Signaling
  • 3.3 Na/H Exchange Regulatory Factor Control of Parathyroid Hormone Receptor Signaling
  • 4. PHYSIOLOGICAL ACTIONS OF PARATHYROID HORMONE
  • 4.1 Mineral Ion Homeostasis
  • 4.2 Na/H Exchange and pH
  • 4.3 Regulation of Vitamin D Synthesis
  • 4.4 Intermediary Metabolism
  • 4.4.1 Gluconeogenesis
  • 4.4.2 Ammoniagenesis
  • 5. DISORDERED PARATHYROID HORMONE REGULATION?IN CHRONIC KIDNEY DISEASE
  • Acknowledgments
  • References
  • 31 - Endocrine Regulation of Phosphate Homeostasis
  • 1. INTRODUCTION
  • 2. PHOSPHATE HOMEOSTASIS
  • 2.1 Intestinal Phosphate Absorption
  • 2.2 Renal Phosphate Reabsorption
  • 2.3 Skeletal Phosphate Resorption
  • 3. ENDOCRINE REGULATORY FACTORS
  • 3.1 Parathyroid Hormone
  • 3.2 Vitamin D
  • 3.3 Fibroblast Growth Factor 23 and Klotho
  • 4. DYSREGULATION OF PHOSPHATE HOMEOSTASIS
  • 4.1 Genetic Disorders of Phosphate Regulation
  • 4.2 Conditions Associated With Phosphate Toxicity
  • 4.2.1 Chronic Kidney Disease
  • 4.2.2 Vascular Calcification
  • 4.2.3 Tumorigenesis and Premature Aging
  • 5. CONCLUSION
  • References
  • Index
  • A
  • B
  • C
  • D
  • E
  • F
  • G
  • H
  • I
  • J
  • K
  • L
  • M
  • N
  • O
  • P
  • Q
  • R
  • S
  • T
  • U
  • V
  • W
  • X
  • Z
  • Back Cover

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