Manual of Pediatric Nephrology

Name: Manual of Pediatric Nephrology
Brand: Springer
Price: 139.09 EUR
Availability: OnlineOnly

Kishore D. Phadke Paul Goodyer Martin Bitzan(Herausgeber*in)

Springer (Verlag)

1. Auflage

Erschienen am 13. Dezember 2013

XV, 630 Seiten

E-Book

PDF mit Wasserzeichen-DRM

Systemvoraussetzungen

978-3-642-12483-9 (ISBN)

139,09 €inkl. 7% MwSt.

Systemvoraussetzungen

für PDF mit Wasserzeichen-DRM

E-Book Einzellizenz

Als Download verfügbar

Beschreibung

Weitere Details

Weitere Ausgaben

Personen

Inhalt

Intro
Manual of Pediatric Nephrology
Copyright Page
Foreword I
Foreword II
Preface
Contents
Abbreviations
1: Evaluation of Renal Disease
1.1 History and Physical Examination
1.2 Dysmorphic Features, Organs, Systems, and Kidney Involvement
1.2.1 Dysmorphic Features and Kidneys
1.2.2 Cardiovascular Diseases and Kidneys
1.2.3 Developmental Delay and Kidneys
1.2.4 Orofacial Disorders and Kidneys
1.2.5 Eyes and Kidneys
1.2.6 Hepatic and Gastrointestinal Diseases and Kidneys
1.2.7 Respiratory System and Kidneys
1.2.8 Skin and Kidneys
1.3 Urine Analysis
1.3.1 Standardized Method for Processing Urine
1.3.2 Examining the Supernatant
1.3.2.1 Color
1.3.2.2 Odor
1.3.2.3 Relative Density
Specific Gravity
Osmolality
Refractometry
1.3.2.4 pH
1.3.2.5 Proteins
Urine Dipstick
Turbidimetric Method
Heat Coagulation Test
Sulfosalicylic Acid (SSA) Test
Quantification of Protein
1.3.2.6 Glucose
1.3.2.7 Blood
1.3.2.8 Ketones
1.3.2.9 Nitrate Reduction Test
1.3.2.10 Leukocyte Esterase Test
1.3.3 Examining the Sediment
1.3.3.1 Cells
1.3.3.2 Lipids
1.3.3.3 Casts
1.3.3.4 Crystals
Types of Crystals
1.3.3.5 Microorganisms
1.4 Assessment of Glomerular Functions
1.4.1 Serum Creatinine (Cr)
1.4.2 Blood Urea
1.4.3 Creatinine Clearance (CrCl)
1.4.4 GFR Estimation
1.5 Assessment of Tubular Functions
1.5.1 Fractional Excretion of Sodium (FeNa)
1.5.2 Tubular Handling of Phosphate
1.5.3 Transtubular Potassium Gradient (TTKG)
1.5.3.1 Interpretation of TTKG Values
1.5.4 Aminoaciduria
1.5.5 Measurement of Urinary Ammonium Excretion
1.5.5.1 Urine Anion Gap
1.5.5.2 Urine Osmolar Gap
1.5.6 Ammonium Chloride Loading Test
1.5.7 Furosemide Test
1.5.8 Bicarbonate Loading Test
1.5.9 Fractional Excretion of Bicarbonates
1.5.10 Tubular (Low Molecular Weight) Proteinuria
1.5.11 Water Deprivation and Vasopressin (ADH) Test
1.6 Histopathological Evaluation
1.6.1 Indications for Kidney Biopsy
1.6.2 Adequacy of the Renal Biopsy
1.6.3 Interpretation of Renal Biopsy
1.6.3.1 Light Microscopy
1.6.3.2 Immuno uorescent (IF) Microscopy
1.6.3.3 Electron Microscopy
1.6.4 Biopsy findings in various common disease conditions
Minimal Change Nephrotic Syndrome
Focal Segmental Glomerulosclerosis (FSGS)
IgM Nephropathy
Membranoproliferative or Mesangiocapillary Glomerulonephritis (MPGN)
Membranous Glomerulopathy
Congenital Nephrotic Syndrome (CNS)
Postinfectious Glomerulonephritis
Crescentic Glomerulonephritis (Proliferative Extra-Capillary)
IgA Nephropathy
Lupus Nephritis
Thrombotic Microangiopathy
Alport Syndrome
Transplant Biopsy
1.7 Radiological Evaluation
1.7.1 Ultrasonography
1.7.1.1 Interpreting a Renal Ultrasound Report
Number and Location of Kidneys
Size of Kidneys
Renal Parenchymal Architecture
Renal Collecting System
Ureters
Bladder
1.7.2 Doppler Studies
1.7.3 Plain Abdominal X-Ray
1.7.4 Voiding Cystourethrogram (VCUG)
1.7.5 Intravenous Urography (IVU)
1.7.6 Nuclear Medicine Investigations
1.7.6.1 Direct Radionuclide Cystography (DRCG)
1.7.6.2 Indirect Radionuclide Cystography
1.7.6.3 Radionuclide Scintigraphy
1.7.7 Choice of Radionuclides in Renal Imaging
1.7.7.1 DMSA Cortical Scintigraphy
1.7.7.2 Dynamic Renography (DTPA or MAG3 Scan)
Procedure
1.7.7.3 Diuretic Renogram
1.7.8 CT (Computed Tomography) Scan
1.7.8.1 Indications
1.7.9 PET/CT Scan
1.7.10 Magnetic Resonance Urography (MRU) and Angiography (MRA)
1.7.11 Arteriography and Venography
1.8 Molecular Genetics
1.8.1 Patterns of Inheritance
1.8.1.1 Mendelian Inheritance
1.8.1.2 Non-Mendelian Inheritance
Strategies for Gene Discovery in Renal Diseases
Genes Involved in Human Renal Diseases
Molecular Genetic Evaluation of Kidney Disease
Samples for DNA Analysis
Molecular Genetics Report
Genetically Inherited Renal Diseases
1.8.2 Nephrotic Syndrome (NS)
1.8.2.1 Isolated NS
1.8.2.2 Syndromic NS
1.8.2.3 Renal Tubular Acidosis
1.8.2.4 Bartter Syndrome
1.8.2.5 Hypomagnesemia
1.8.2.6 Nephrogenic Diabetes Insipidus
1.8.2.7 Central Diabetes Insipidus
1.8.2.8 Dent's Disease
1.8.2.9 Hemolytic Uremic Syndrome
1.8.2.10 Monogenic Forms of Hypertension
1.8.3 Cystic Kidney Diseases
1.8.3.1 Polycystic Kidney Disease
1.8.3.2 Nephronophthisis
1.8.3.3 Alport Syndrome
1.8.3.4 List of Human Malformation Syndromes with Kidney Hypoplasia/Dysplasia
1.8.3.5 Common Chromosomal Disorders Associated with Renal Agenesis/Hypoplasia
Suggested Reading
2: Fluids, Electrolytes, and Acid-Base Disorders
2.1 Acid Base and the Kidney
2.1.1 Interpretation of Blood Gas Abnormalities
2.1.1.1 Overview of Acid-Base Physiology
2.1.2 Arterial Blood Gas Analysis
2.1.2.1 General Aspects
2.1.2.2 Collecting Blood Sample for ABG
2.1.2.3 Terminologies
2.1.2.4 Calculations
Anion Gap (AG)
Delta Ratio (?/?) (see Table 2.3)
2.1.2.5 Normal Values of ABG
2.1.2.6 Interpreting a Blood Gas
2.1.2.7 The Summary of Approach to ABG Interpretation
2.1.2.8 Using the Nomogram for the Diagnosis of Acid-Base Disorder
2.1.2.9 Case Example
2.1.2.10 Physiochemical Approach to Acid-Base Disorders (Stewart's Approach)
2.1.2.11 Case Example Using Stewart's Approach
2.1.3 Metabolic Acidosis
2.1.3.1 Etiology
2.1.3.2 Consequences of Metabolic Acidosis
Acute Metabolic Acidosis
Chronic Metabolic Acidosis
2.1.3.3 Clinical Features
2.1.3.4 Evaluation
2.1.3.5 Approach to Metabolic Acidosis
2.1.3.6 Management
Bicarbonate Therapy
Tris-Hydroxymethyl Aminomethane (THAM)
Hemodialysis (HD) or Peritoneal Dialysis (PD)
2.1.4 Metabolic Alkalosis
2.1.4.1 Etiology
2.1.4.2 Phases of Metabolic Alkalosis
Initiation
Maintenance
2.1.4.3 Clinical Features
2.1.4.4 Evaluation
2.1.4.5 Approach to Metabolic Alkalosis
2.1.4.6 Management
Chloride-Responsive Metabolic Alkalosis
Chloride-Resistant Metabolic Alkalosis
Treatment of Refractory Metabolic Alkalosis
2.2 Sodium and Water Balance
2.2.1 Sodium Handling and Dysnatremias
2.2.1.1 Renal Handling of Sodium
2.2.2 Hyponatremia
2.2.2.1 Applied Physiology
2.2.2.2 Etiology
2.2.2.3 Clinical Features
2.2.2.4 Evaluation
2.2.2.5 Approach to Hyponatremia
2.2.2.6 Treatment
2.2.2.7 Case Example for Correction of Hyponatremia
2.2.3 Syndrome of Inappropriate Antidiuresis
2.2.3.1 Diagnostic Criteria (Bartter and Schwartz 1967)
2.2.3.2 Etiology
2.2.3.3 Evaluation and Differential Diagnosis
2.2.3.4 Treatment
2.2.4 Hypernatremia
2.2.4.1 Etiology
2.2.4.2 Clinical Features
2.2.4.3 Evaluation
2.2.4.4 Treatment
2.2.4.5 Approach to Hypernatremia
2.2.4.6 Case Example for Correction of Hypernatremia
2.3 Disorders of Potassium Homeostasis
2.3.1 Potassium Balance
2.3.1.1 Renal Handling of Potassium
Cortical Collecting Duct
Medullary Collecting Duct
2.3.1.2 Urinary Indices Used in Evaluation of Disorders of Potassium Homeostasis
2.3.2 Hypokalemia
2.3.2.1 Applied Physiology
2.3.2.2 Etiology
2.3.2.3 Clinical Features
2.3.2.4 Evaluation
2.3.2.5 Approach to Hypokalemia
2.3.2.6 Approach to Hypokalemia Due to Increased Renal Losses
2.3.2.7 Treatment of Hypokalemia
Symptomatic Hypokalemia
Management in Nonemergent Situations
Asymptomatic Hypokalemia
Formulations of Potassium Salts Available in the Market
2.3.3 Hyperkalemia
2.3.3.1 Etiology
2.3.3.2 Clinical Features
2.3.3.3 Evaluation
2.3.3.4 Approach to Hyperkalemia
2.3.3.5 Treatment
Immediate Treatment (Also See Chap. 8)
Long-Term Treatment
2.4 Calcium, Phosphate and Magnesium
2.4.1 Calcium Disturbances
2.4.1.1 Calcium Metabolism
Introduction
Renal Handling of Calcium
2.4.1.2 Hypocalcemia
Definition
Etiology
Clinical Features (See Table 2.10)
Eliciting Signs of Chvostek and Trousseau
Chvostek's Sign
Trousseau's Sign
Evaluation of Hypocalcemia
Approach to Hypocalcemia
Treatment
2.4.1.3 Hypercalcemia
Definition
Etiology
Clinical Features
Clinical Features of Hypercalcemia
Evaluation
Approach to Hypercalcemia
Treatment
2.4.1.4 Hypercalciuria
Evaluation of Hypercalciuria
Approach to Hypercalciuria
Idiopathic Hypercalciuria
Clinical Features
Treatment
Genetic Conditions Associated with Hypercalciuria
2.4.2 Disorders of Phosphate Metabolism
2.4.2.1 Hypophosphatemia
2.4.2.2 Etiology
2.4.2.3 Clinical Features
2.4.2.4 Clinical Features of Hypophosphatemia
2.4.2.5 Evaluation
2.4.3 Rickets
2.4.3.1 Overview
2.4.3.2 Sources of Vitamin D and Its Metabolism
2.4.3.3 Etiology
2.4.3.4 Diagnosis and Evaluation of Rickets
Symptoms and Clinical Signs
Nutritional Rickets
Non-nutritional Rickets
Biochemical Parameters
Biochemical Profile at Different Stages of Nutritional Rickets
Radiological Findings
2.4.3.5 Treatment
Nutritional Rickets
Prevention of Nutritional Rickets
Non-nutritional Rickets
2.4.3.6 Vitamin D-Dependent Rickets (VDDR)
VDDR Type I Rickets
VDDR Type II Rickets
2.4.4 Magnesium
2.4.4.1 Renal Handling of Magnesium
2.4.4.2 Hypomagnesemia
2.4.4.3 Etiology
2.4.4.4 Clinical Features
Symptoms and Signs of Hypomagnesemia
2.4.4.5 Evaluation
Fractional Excretion of Magnesium (FeMg)
2.4.4.6 Clinical and Biochemical Features of Genetic Disorders of Magnesium Handling
2.4.4.7 Treatment
Available Preparations
2.4.4.8 Hypermagnesemia
2.5 Fluid Therapy in Select Situations
2.5.1 Maintenance Intravenous Fluids
2.5.2 Fluid Therapy in Diabetic Ketoacidosis (DKA)
Fluid Resuscitation
Electrolyte Replacement
Potassium
Sodium
Phosphate
Magnesium
Correction of Acidosis
Identification of Early Features of Cerebral Edema and Treatment
2.5.3 Fluid Therapy in Shock
Types of Shock
Management of a Child with Shock
Management of Shock in PICU
Dopamine
Dobutamine
Epinephrine
Norepinephrine
Milrinone
Vasopressin
2.5.4 Fluid Therapy in Acute Diarrhea
History
Rehydration Therapy
Oral Rehydration Solutions (ORS) see Table 2.9
Treatment According to Severity of Dehydration (Also See Table 2.8)
Plan A
Plan B
Plan C
2.5.5 Management of Dehydration and Shock in a Malnourished Child
Challenges in Managing Malnourished Children with Dehydration and Shock
Management of Dehydration
Management of Shock
F-75 and F-100 Diet
Suggested Reading
3: Glomerular Diseases
3.1 Approach to Hematuria
3.1.1 Abstract
3.1.2 Definitions
3.1.3 Introduction
Box 3.1 Etiology of Hematuria
3.1.4 Baseline Investigations for Hematuria
3.1.5 Management
3.2 Approach to Proteinuria
3.2.1 Abstract
3.2.2 Introduction
3.2.3 Definitions
Box 3.2 Etiology of Proteinuria
3.2.4 Proteinuria Methods
3.2.5 Clinical Signs and Symptoms
3.2.6 Basic Investigations
3.3 Primary Nephrotic Syndrome
3.3.1 Idiopathic Nephrotic Syndrome (INS)
3.3.1.1 Introduction
3.3.1.2 Definitions
3.3.1.3 Pathology o f Idiopathic Nephrotic Syndrome (INS)
3.3.1.4 Clinical Features
Typical Presentation
Atypical Features of Nephrotic Syndrome Suggesting Alternative Diagnoses
3.3.1.5 Investigations at First Presentation of Nephrotic Syndrome
Box 3.4 Indications for Renal Biopsy in Patients with Nephrotic Syndrome
3.3.1.6 Treatment of Idiopathic Nephrotic Syndrome
First Episode
Relapse Treatment
Frequent Relapses and Glucocorticoid (Steroid) Dependence
Glucocorticoid Adverse Effects
Second-Line Agents and Strategies (Fig. 3.6)
Management of Glucocorticoid (Steroid)-Resistant Idiopathic Nephrotic Syndrome (SRNS)
Adjunctive Therapies
Management of Edema, Fluid Balance, and Hypertension
Complications in Children with Primary Nephrotic Syndrome
Infections
Hypercoagulopathy
Acute Kidney Injury
Electrolyte Disturbances
3.3.1.7 Prognosis
3.3.1.8 Long-Term Management of Children with Nephrotic Syndrome
Nutrition
Immunization of the Child with Nephrotic Syndrome
Adrenal Suppression and Dosing of Glucocorticoids During Stress
3.3.1.9 Support and Information for Patients and Families
Box 3.5 Recommendations for Patients with Adrenal Insufficiency
3.3.2 Minimal Change Nephrotic Syndrome (MCNS)
3.3.3 Focal Segmental Glomerulosclerosis (FSGS)
3.3.4 Inherited Forms of Nephrotic Syndrome
3.3.4.1 Introduction
3.3.4.2 Congenital Nephrotic Syndrome (CNS)
Box 3.6 Etiologies of Congenital Nephrotic Syndromes
3.3.4.3 Finnish-Type Congenital Nephrotic Syndrome (FCNS)
3.3.4.4 Denys-Drash Syndrome (DDS)
3.3.4.5 Frasier Syndrome (FS)
3.3.4.6 WAGR Syndrome
3.3.4.7 Pierson Syndrome (PS)
3.4 Acute Glomerulonephritis
3.4.1 Acute Post-Infectious (Poststreptococcal) Glomerulonephritis (APIGN/APSGN)
3.4.1.1 Abstract
3.4.1.2 Introduction
Vignette
3.4.1.3 Definition
3.4.1.4 Epidemiology
3.4.1.5 Etiology and Pathogenesis
3.4.1.6 Clinical Features
3.4.1.7 Laboratory Investigations
3.4.1.8 Kidney Biopsy
3.4.1.9 Treatment of APIGN
3.4.1.10 Prognosis and Outcome
3.4.2 Infection-Induced Immune Complex Glomerulonephritis (ICGN)
Vignette (1)
Vignette (2)
3.4.2.1 Abstract
3.4.2.2 Definition
3.4.2.3 Etiology and Pathogenesis
3.4.2.4 Clinical Features
3.4.2.5 Investigations
3.4.2.6 Treatment
3.4.2.7 Prognosis and Outcome
3.4.3 Rapidly Progressive Glomerulonephritis (RPGN)
3.4.3.1 Definition
Vignette
3.4.3.2 Etiology and Pathogenesis
Box 3.7 Classification of RPGN
3.4.3.3 Pathogenesis of Crescent Formation
3.4.3.4 Clinical Features
3.4.3.5 Investigations
3.4.3.6 Renal Histopathology
3.4.3.7 Treatment
3.4.3.8 Prognosis
3.5 Chronic Glomerulonephritis and Immune Nephropathies
3.5.1 Membranoproliferative Glomerulonephritis
Box 3.8 Traditional Classification of Membranoproliferative Glomerulonephritis (MPGN)
Box 3.10 Anti-Neutrophil Cytoplasmic Antibodies (ANCA)
3.5.1.1 Etiology and Pathogenesis
3.5.1.2 Clinical Presentation
3.5.1.3 Laboratory Evaluation
3.5.1.4 Therapy
3.5.1.5 MPGN Type 1
Prognosis
3.5.1.6 Type II MPGN (Dense Deposit Disease)
Clinical Features
Prognosis
3.5.1.7 MPGN Type III
3.5.2 IgA Nephropathy
3.5.2.1 Abstract
3.5.2.2 Introduction
3.5.2.3 Definition
Vignette
3.5.2.4 Etiology and Pathogenesis
3.5.2.5 Clinical Features
3.5.2.6 Laboratory Investigations
3.5.2.7 Pathological Diagnosis
3.5.2.8 Therapeutic Management
3.5.2.9 Prognosis
3.5.3 Membranous Nephropathy (MN)
3.5.3.1 Introduction
3.5.3.2 Etiology and Pathogenesis
3.5.3.3 Clinical Features
3.5.3.4 Laboratory Investigations
3.5.3.5 Histopathology (Table 3.18)
3.5.3.6 Therapeutic Management
3.5.3.7 Prognosis
3.5.4 C1q Nephropathy
3.5.4.1 Definition
3.5.4.2 Etiology and Pathogenesis
3.5.4.3 Clinical Signs and Symptoms
3.5.4.4 Investigations
3.5.4.5 Approach and Management
3.5.4.6 Prognosis and Outcome
3.6 Systemic Vasculitis Affecting the Kidney
3.6.1 Abstract
3.6.2 Definitions
Box 3.9 Classification of Childhood Vasculitis a
3.6.3 Schönlein-Henoch Purpura Nephritis
3.6.3.1 Abstract
3.6.3.2 Definition
3.6.3.3 Etiology and Pathogenesis
3.6.3.4 Clinical Features of SHN
3.6.3.5 Laboratory Investigations (see Table 3.19)
3.6.3.6 Renal Histopathology
3.6.3.7 Treatment
Patient Monitoring
Medication Therapy of SHP/SHN
3.6.3.8 Prognosis and Outcome
3.6.4 ANCA-Associated Vasculitis (AAV)
3.6.4.1 Definitions
3.6.4.2 Clinical Presentation of AAV
3.6.4.3 Microscopic Polyangiitis (MPA)
3.6.4.4 Granulomatosis with Polyangiitis (GPA, Wegener's Granulomatosis)
3.6.4.5 Eosinophilic Granulomatosis with Polyangiitis (EGPA
former Churg-Strauss Syndrome)
3.6.4.6 Renal Histopathology of ANCA-Associated Vasculitis
3.6.4.7 Treatment of ANCA Vasculitis
3.6.4.8 Outcome
3.6.5 Lupus Nephritis (LN)
3.6.5.1 Definition
Box 3.11 American Rheumatology Association Criteria for SLE (1982) a
Box 3.12 American College of Rheumatology Guideline Recommendations for the Diagnosis and Treatment of Lupus Nephritis
3.6.5.2 Pathogenesis
3.6.5.3 Clinical Features
Extrarenal
Renal
3.6.5.4 Laboratory Investigations
3.6.5.5 Renal Histopathology
Box 3.13 WHO Morphologic Classification of Lupus Nephritis (Modified in 1982)
Box 3.14 International Society of Nephrology/Renal Pathology Society (ISN/RPS) Classification of Lupus Nephritis (2003) a
Box 3.15 Active and Chronic Glomerular Lesions as Defined in the ISN/RPS 2003 Classification of Lupus Nephritis
3.6.5.6 Treatment
3.6.5.7 Prognosis
Poor Prognostic Factors
3.6.5.8 Renal Transplantation
3.6.6 Other Vasculitides
3.6.6.1 Takayasu Arteritis
3.6.6.2 Childhood Polyarteritis Nodosa (cPAN)
3.6.6.3 Kawasaki Disease (KD)
3.7 Hemolytic Uremic Syndrome/Thrombotic Microangiopathies
3.7.1 Introduction and Definitions
Box 3.16 Thrombotic Microangiopathies (TMA)
3.7.2 Approach to a Patient with HUS
Box 3.17 Six Key Questions
3.7.3 Typical (Enteropathic/STEC) HUS
3.7.4 Pneumococcal (Neuraminidase-Induced) HUS (pnHUS)
3.7.5 Atypical (Complement-Induced) HUS (aHUS)
3.7.6 Treatment of Atypical HUS
3.7.6.1 Plasma Therapy
Exceptions from PLEX Initiation Recommendations
Withdrawal from PLEX Therapy
Rationale for Plasma Exchange
3.7.6.2 Alternative Treatment Strategies
3.7.6.3 Anti-C5 Monoclonal Antibody Therapy
3.7.7 Renal Transplantation in HUS
3.8 Other Inherited Glomerular Diseases
3.8.1 Alport Syndrome
3.8.1.1 Introduction
3.8.1.2 Etiopathogenesis
3.8.1.3 Clinical Features
3.8.1.4 Laboratory Evaluation
3.8.1.5 Histopathology
3.8.1.6 Treatment
3.8.2 Thin Basement Membrane Disease
Suggested Reading
4: Tubular Disorders
4.1 An Approach to Renal Tubulopathies
4.2 An Approach to Polyuria
4.2.1 Causes of Polyuria
4.2.1.1 Acquired Dysfunction of Salt/Water Reabsorption
4.2.1.2 Hereditary Tubulopathies Affecting Salt Reabsorption
4.2.1.3 Abnormal Production of ADH or Resistance to ADH
4.2.2 Clinical Features
4.3 Diabetes Insipidus
4.3.1 Nephrogenic DI (NDI)
4.3.1.1 Etiology
4.3.1.2 Clinical Presentation
4.3.1.3 Diagnosis
4.3.1.4 Treatment
4.3.2 Central Diabetes Insipidus (CDI)
4.3.2.1 Etiology
4.4 Renal Tubular Acidosis
4.4.1 Classification of RTA
4.4.2 Etiology
4.4.2.1 Distal RTA
4.4.2.2 Proximal RTA
4.4.2.3 Type IV RTA
4.4.3 Clinical Features
4.4.4 Investigations
4.4.5 Treatment
4.4.6 Fanconi Syndrome
4.4.6.1 Etiology
Congenital Causes
Acquired Causes
4.5 Bartter and Gitelman Syndrome
4.5.1 Bartter Syndrome
4.5.1.1 Pathophysiology
4.5.1.2 Presentation
4.5.1.3 Treatment
4.5.2 Gitelman Syndrome
4.6 Nephropathic Cystinosis
4.7 Hypophosphatemic Rickets
4.7.1 X-Linked Hypophosphatemic (XLH) Rickets
4.7.2 Other Hereditary Forms of Hypophosphatemic Rickets
4.8 Primary Hyperoxaluria (PH)
4.8.1 Primary Hyperoxaluria (PH) Type 1
4.8.2 Type 2 Hyperoxaluria
4.9 Miscellaneous Tubular Disorders
4.9.1 Pseudohypoaldosteronism
4.9.2 Cystinuria
4.9.3 Lowe Syndrome
4.10 Tubulointerstitial Nephritis
4.10.1 Acute Tubulointerstitial Nephritis (Acute TIN)
4.10.1.1 Etiology
4.10.1.2 Clinical Presentation
4.10.1.3 Investigations
4.10.1.4 Treatment
4.10.1.5 Prognosis
4.10.2 Chronic Tubulointerstitial Nephritis
4.10.2.1 Etiology
4.10.2.2 Clinical Features
4.10.2.3 Treatment and Prognosis
Suggested Reading
5: Cystic Renal Diseases
5.1 Definitions
5.2 Introduction
5.3 Autosomal Dominant Polycystic Kidney Disease (ADPKD)
5.3.1 Extrarenal Manifestations
5.3.2 Diagnosis
5.3.3 Family Screening
5.3.4 Patient Monitoring
5.3.5 Treatment
5.4 Autosomal Recessive Polycystic Kidney Disease (ARPKD)
5.4.1 Extrarenal Manifestations
5.4.2 Treatment
5.4.3 Monitoring
5.5 Nephronophthisis (NPHP)
5.5.1 NPHP Type 1
5.5.2 NPHP Type 2 (Infantile Form)
5.6 Medullary Cystic Kidney Disease (MCKD)
5.7 Multicystic Dysplastic Kidneys (MCDK)
5.8 Simple Renal Cysts
Suggested Reading
6: Issues Related to Pediatric Urology
6.1 Antenatal Diagnosis of Renal Diseases
6.1.1 Fetal Urine Production
6.1.2 Nephrogenesis
6.1.3 Imaging the Fetal Urinary Tract
6.1.4 Fetal Genitourinary Ultrasound Assessment
6.1.5 When to Refer Antenatally?
6.1.6 Why Refer Antenatally?
6.1.7 When to Evaluate Hydronephrosis Postnatally?
6.1.8 Recommendations for Postnatal Referral
6.1.9 Ultrasound Findings Suggestive of Renal Disease
6.1.9.1 Number of Kidneys
6.1.9.2 Renal Position
6.1.9.3 Echogenicity of Kidneys
6.1.9.4 Size of Kidneys
6.1.9.5 Antenatal Hydronephrosis
Postnatal Evaluation of Antenatal Hydronephrosis
6.1.9.6 Renal Cysts
6.1.9.7 Renal Tumors
6.1.9.8 Ureteric Dilatation
6.1.9.9 Bladder Abnormalities
6.1.9.10 Miscellaneous
6.2 Congenital Hydronephrosis and Hydroureter
6.2.1 Definitions
6.2.2 Postnatal Evaluation of Hydronephrosis
6.2.3 VCUG: Common Pitfalls
6.2.4 MAG3-Furosemide Renogram (Diuretic Renogram)
6.2.5 Ancillary Tests (Not Routinely Indicated)
6.3 Congenital Malformations of the Kidney and Urinary Tract
6.3.1 Duplex Kidneys
6.3.2 Ureterocele
6.3.3 Anomalies of the Lower Urinary Tract
6.3.3.1 Bladder Exstrophy-Epispadias Complex
Incidence
Clinical Presentations
Immediate Management
Management
6.3.3.2 Hypospadias
Classification
Clinical Findings
Indications for Intersex Work-Up
Management
Prognosis
6.4 Posterior Urethral Valves (PUV)
6.4.1 Clinical Presentations
6.4.2 Effects on the Urinary Tract and Kidneys
6.4.3 Pop-Off Mechanisms to Relieve Bladder Pressure
6.4.4 Evaluation
6.4.5 Differential Diagnosis of the Dilated Bladder on Ultrasound
6.4.5.1 Bladder Level Causes
6.4.5.2 Urethral Level Causes
6.4.6 Management
6.4.7 Complications of PUV
6.4.8 Why Does PUV Lead to Chronic Kidney Disease?
6.4.9 Predictors of a Poor Renal Function
6.4.9.1 Antenatal
6.4.9.2 Postnatal
6.4.10 Prune Belly Syndrome (PBS)
6.5 Urinary Tract Infections
6.5.1 Introduction
Box 6.1 Urinary tract infection (UTI) definitions
6.5.2 Etiopathogenesis
6.5.3 Clinical Features
6.5.4 Diagnosis
6.5.5 Tests That Help Improve the Predictive Value of UTI
6.5.6 Imaging
6.5.7 Management
6.5.8 Recurrent UTI
6.5.9 Chemoprophylaxis for Urinary Tract Infections
6.5.9.1 The Evidence Base for Chemoprophylaxis
6.5.9.2 Long-Term Follow-Up
6.6 Vesicoureteral Re ux
6.6.1 Grading of VUR
6.6.1.1 Indications for Surgical Treatment
6.6.2 Screening for VUR in the Sibling
6.6.3 VUR and Circumcision
6.6.4 Newer Interventions for VUR
6.6.5 Outcome
6.7 Neurogenic Bladder Dysfunction
Box 6.2 Causes of neurogenic bladder dysfunction in children
6.7.1 Sacral Agenesis
6.7.2 Anorectal Malformation
6.7.3 Cerebral Palsy
6.7.4 Spinal Injury
6.7.5 Spinal Dysraphism
6.7.5.1 Occult Spinal Dysraphism
Box 6.3 Spinal dysraphism - initial assessment of the newborn
6.7.6 Approach to a Child with Neurogenic Bladder Dysfunction
6.7.7 Management
6.7.7.1 Anticholinergic Medications and Clean Intermittent Catheterization (CIC)
6.7.7.2 Cutaneous Vesicostomy
6.7.7.3 Botulinum Toxin-A
6.7.7.4 Bladder Augmentation
Box 6.4 Techniques for bladder augmentation
Management Issues Following Augmentation
6.7.7.5 Continent Catheterizable Conduits
6.7.7.6 Bladder Outlet Management (Continence Procedures)
Box 6.5 Options for management of the bladder neck
6.7.8 Other Associated Issues in Spinal Dysraphism
6.8 Voiding Dysfunction
6.8.1 Lower Urinary Tract Symptoms
6.8.2 Investigations for Evaluation of Functional Bladder Abnormalities
6.8.2.1 Elimination Diary
6.8.2.2 Measurement of Urine Flow and Residual Urine
Box 6.7 Bladder calculations
6.8.2.3 Urodynamic Studies (UDS)/Cystometry
Filling Phase
Voiding Phase
Procedure
6.8.3 Various Presentations of "Voiding Dysfunction"
6.8.3.1 Associated Symptoms
6.8.4 Different Types of Voiding Dysfunction (Non-neurogenic Disorders of Voiding)
6.8.5 Treatment Options for Voiding Dysfunction
6.9 Enuresis
6.9.1 Introduction
6.9.2 Terminologies
6.9.3 Guidelines to Approach
6.9.4 Management
6.9.4.1 Counseling
6.9.4.2 First-Line Therapy: Alarm Device Therapy (Level of Evidence 1)
6.9.4.3 First-Line Therapy: Desmopressin Therapy (Level of Evidence 1)
6.9.4.4 Therapy-Resistant Enuresis
Box 6.8 Stepwise management of enuresis
6.9.4.5 Summary of Evidence-Based Management
6.9.5 Conclusion
6.10 Stone Disease (Urolithiasis)
6.10.1 Introduction
6.10.2 Epidemiology
6.10.3 Etiology and Risk Factors
6.10.3.1 Metabolic Factors
6.10.3.2 Dietary Factors
6.10.3.3 Urinary Tract Infection
6.10.3.4 Genetic Factors
6.10.3.5 Other Factors
6.10.4 Pathogenesis
6.10.5 Clinical Features
6.10.6 Evaluation
6.10.6.1 History and Examination
6.10.6.2 Imaging
6.10.6.3 Metabolic Tests
6.10.6.4 Stone Analysis
6.10.7 Treatment
6.10.7.1 Medical Therapy
Acute Management
Diet and Fluids
Medications
6.10.7.2 Surgical Treatment
6.11 Kidney Trauma
6.11.1 Natural Protection and Predisposition
6.11.2 Etiology and Mechanism of Injury
6.11.3 Complications
6.11.4 Clinical Findings
6.11.4.1 Symptoms
6.11.4.2 Signs
6.11.5 Laboratory Findings
6.11.6 Imaging Findings
6.11.6.1 Indications
6.11.6.2 Modalities
6.11.7 Grading of Renal Trauma
6.11.8 Treatment
6.11.9 Prognosis and Follow-Up
Suggested Reading
7: Hypertension
7.1 Introduction
7.2 Definitions
Box 7.1 Definitions: Pediatric Hypertension
7.3 Etiology of Hypertension
7.4 Clinical Signs and Symptoms
7.5 Approach to the Child and Adolescent with Hypertension
7.5.1 Standardized BP Measurement and Confirmation of Hypertension
7.5.2 Evaluate for End-Organ Injury
7.5.3 Differentiate Between Primary and Secondary Hypertension
7.5.4 When to Suspect Monogenic Hypertension
7.6 Investigations
7.6.1 Investigations for Mild-to-Moderate Hypertension
7.6.2 Investigations for Moderate-to-Severe (Stage 2) Hypertension
7.6.3 Diagnose Underlying Cause for Secondary Hypertension
Box 7.2 Investigations in Children and Adolescents with Hypertension
7.7 Home (HBPM) and Ambulatory BP Monitoring (ABPM)
7.7.1 How to Perform ABPM?
7.7.2 Interpretation of ABPM Studies, Calculations, and Nocturnal Dipping
7.7.3 Indications for ABPM Studies
7.7.4 White Coat Hypertension (WCH) and Masked Hypertension (MH)
7.8 Management of Children with Hypertension
7.8.1 Treatment Indications and Goals
7.8.2 Management of Hypertension Based on BP Staging
7.8.3 Stepwise Approach to Managing Primary Hypertension
Box 7.3 Non-pharmacological Treatment of Primary Hypertension a
7.8.4 Pharmacological Therapies of Primary and Secondary Hypertension
7.8.4.1 Principles of Antihypertensive Pharmacotherapy
7.8.4.2 "ACD" Strategy
7.8.5 Presentation and Management of Hypertensive Crises
7.8.5.1 Hypertensive Emergencies: Diagnosis and Treatment
7.8.5.2 Hypertensive Urgencies: Diagnosis and Treatment
7.8.5.3 Complications of (Acute) Severe Hypertension
Hypertensive Encephalopathy
Posterior Reversible (Leuko)Encephalopathy Syndrome (PRES)
7.8.6 Treatment of Acute and Severe Hypertension
7.8.6.1 Approach to Hypertensive Emergencies and Urgencies Due to APIGN/APSGN
7.9 Prognosis
Vignettes
Suggested Reading
Web Links
8: Acute Kidney Injury
8.1 Definition and Incidence
8.2 Classification and Staging System for AKI
8.3 Etiology
8.3.1 Prerenal Causes (Inadequate Renal Perfusion)
8.3.1.1 Decreased True Intravascular Volume
8.3.1.2 Decreased Effective Circulating Volume
8.3.2 Renal Causes (Intrinsic Renal Disease)
8.3.3 Postrenal Causes
8.3.4 AKI in Developing Countries Versus the Developed World
8.4 Approach and Evaluation
8.4.1 Medical History
8.4.2 Physical Examination
8.4.3 Laboratory Evaluation
8.4.3.1 Hematology
8.4.3.2 Biochemistry
8.4.3.3 Urine Analysis
8.4.3.4 Microbiology, Serology and Immunology
8.4.3.5 Imaging
8.4.3.6 Renal Biopsy
8.4.3.7 Fluid Challenge Test
8.5 Management of AKI
8.5.1 Renal-Specific Therapy (Dependent on Underlying Etiology)
8.5.2 Renal Supportive Therapy
8.5.3 Renal Replacement Therapy (RRT)
8.5.3.1 Indications for Dialysis
8.5.3.2 Choice of Various Modalities of RRT
8.5.3.3 Factors In uencing the Choice of RRT Modality
8.6 Acute Peritoneal Dialysis (PD)
8.6.1 Indications for Acute Peritoneal Dialysis
8.6.1.1 Renal Indications (AKI with or without Oligoanuria)
8.6.1.2 Non-Renal Indications (with or without AKI)
8.7 Hemodialysis (HD)
8.8 Continuous Renal Replacement Therapies (CRRT)
8.8.1 Nomenclature for CRRT
8.8.2 Advantages of CRRT
8.8.3 Disadvantages of CRRT
8.8.4 Vascular Access for CRRT
8.8.5 CRRT Filter and Machines
8.8.6 Replacement Fluid
8.8.7 Anticoagulation
8.8.8 CRRT Prescription
8.8.9 Complications of CRRT
8.9 Long-term Follow Up of Children with AKI
Suggested Reading
9: Chronic Kidney Disease (CKD)
9.1 Definition of CKD
9.2 Staging of CKD
9.3 Etiology of CKD
9.4 Clinical Presentations
Box 9.1 High Index of Suspicion for CKD
9.4.1 History
9.4.2 Physical Examination
9.4.2.1 Physical Manifestations of a Child with CKD
9.5 Evaluation and Management of CKD
9.5.1 General Aspects
9.5.2 Nutrition and Growth in CKD
9.5.2.1 Assessment of Nutritional Status and Growth
9.5.2.2 Management of Nutrition
9.5.2.3 The Use of Nutritional Supplements
Box 9.2 Tube feeding advancements
9.5.2.4 Management of Growth
9.5.2.5 Growth Hormone Therapy
9.5.3 Anemia of CKD
9.5.3.1 Assessment of Anemia
Box 9.3 Assessment of anemia in CKD
9.5.3.2 Management of Anemia
9.6 Bone Disease in CKD
9.7 Management of Renal Osteodystrophy
9.7.1 Phosphate Control
9.7.2 Correction of Serum Calcium
9.7.2.1 Calcium Supplementation
Dietary Considerations
9.7.2.2 Vitamin D Therapy
Active Vitamin D Therapy
Monitoring
Parathyroidectomy
Indications for Orthopedic Surgery
Metabolic Acidosis
Aluminum Bone Disease
9.7.3 Hypertension
9.7.3.1 Antihypertensive Drugs in CKD
9.7.4 Cardiovascular Morbidity
9.7.5 Infection
9.7.6 Pneumococcal Vaccine
9.7.7 Hematological Issues
9.7.8 Fluid Electrolyte and Acid-Base Issues
9.7.9 Psychosocial Issues
9.8 Retarding Progression of CKD
9.9 Indications for Renal Replacement Therapy
Conclusion
Box 9.4 Summary of KDOQI Recommendations
Suggested Reading
10: Chronic Dialysis
10.1 PD
10.1.1 Introduction
10.1.2 Definitions
10.1.2.1 Principles of PD
10.1.2.2 Types of PD
Box 10.1 Types of PD (the PD Alphabet)
10.1.3 When to Use PD and HD?
10.1.3.1 Advantages of Peritoneal Dialysis
10.1.3.2 Challenges of PD
10.1.3.3 Contraindications to PD
10.1.4 Initiation of PD
10.1.4.1 When to Start Dialysis
10.1.4.2 Education
Box 10.2 Outline of Training for Peritoneal Dialysis (Training Curriculum)
10.1.4.3 PD Catheter Placement and Choice of Catheter
10.1.4.4 Post Catheter Insertion Break-In Protocol
10.1.4.5 Healing of the PD Exit Site
10.1.4.6 Maintenance Dialysis Prescription
10.1.4.7 Choice of PD Solutions
10.1.4.8 Adequacy of Dialysis
10.1.4.9 Peritoneal Equilibration Test (PET) Protocol
10.1.4.10 Chronic Exit Site Care
10.1.4.11 Practical Advice (Rules)
10.1.5 Complications of PD
10.1.5.1 Mechanical Complications
10.1.5.2 Accidental Disconnection Protocol
10.1.5.3 Infectious Complication: PD Associated Peritonitis (PDAP)
Box 10.3 Differential Diagnosis of Cloudy Effluent
10.1.5.4 Empiric Antibiotic Therapy
10.1.5.5 Relapsing Peritonitis
10.1.5.6 PD Catheter-Related Infections
10.1.5.7 Indications for PD Catheter Removal
10.1.5.8 Non-infectious Complications
10.1.5.9 Rare Complications
10.1.6 General Antibiotic Prophylaxis for PD Patients
10.2 Hemodialysis
10.2.1 Principles of HD
10.2.1.1 Solute Clearance
10.2.1.2 Ultrafiltration
10.2.2 Differences between "Pediatric Dialysis" and HD in Adults
10.2.3 Vascular Access
10.2.4 Dialysis Prescription
10.2.5 Complications of HD
10.2.6 Dialysis Adequacy
10.2.7 Causes of Inadequate Dialysis
Suggested Reading
11: Renal Transplantation
11.1 Introduction
11.2 Contraindications to Transplantation
11.3 Pre-transplant Evaluation
11.3.1 Donor
11.3.1.1 Exclusion Criteria for Living Donors
11.3.1.2 Donor Investigations
11.3.1.3 Blood Group, Tissue Typing, and Cross Match
11.3.2 Recipient
11.3.2.1 Investigations
11.3.2.2 Determining the Cause of ESRD
11.3.2.3 Immunization Status
11.4 Preoperative Management
11.5 Intra- and Postoperative Management
11.5.1 Surgery
11.5.2 Fluids and Electrolytes
11.5.3 Monitoring
11.6 Induction and Maintenance Immunosuppression Protocol
11.6.1 Induction Regime
11.6.1.1 Day 0
11.6.2 Postoperative Immunosuppression
11.6.2.1 Days 0-7
11.6.3 Maintenance Immunosuppression
11.6.4 Alternative Drugs for Calcineurin Inhibitor Toxicity or Avoidance (Inhibitors of Mammalian Target of Rapamycin [mTO...
11.7 Posttransplant Complications
11.7.1 Delayed Graft Function (DGF)
11.7.2 Acute Rejection (AR)
Box 11.1 Transplant biopsy: Banff criteria
11.7.3 Infections
Box 11.2 Infections after organ Transplantation
11.7.3.1 CMV Infection
11.7.3.2 Varicella
11.7.3.3 Polyoma BK Virus Infection
11.7.3.4 Prophylaxis
11.7.4 Chronic Allograft Dysfunction (CAD)
11.7.5 Surgical Complications
11.7.6 Metabolic Complications
11.7.7 Recurrence of Disease in Allograft (Table 11.1)
11.7.8 Lymphoproliferative Disease (PTLD)
11.7.9 Hypertension
11.7.10 Growth
11.8 Renal Transplantation in Countries/Regions with Limited Resources
Suggested Reading
12: Oncology and Kidney
12.1 Renal Tumors
12.1.1 Wilms' Tumor
12.1.1.1 Incidence
12.1.1.2 Presentation
12.1.1.3 Evaluation
12.1.1.4 Staging
12.1.1.5 Histopathology
12.1.1.6 Therapy
12.1.1.7 Surgery
12.1.1.8 Chemotherapy
12.1.1.9 Radiation Therapy
12.1.1.10 Bilateral Wilms' Tumor
12.1.1.11 Prognosis
12.1.1.12 Long-Term Concerns Post-therapy for Wilms' Tumor
12.1.2 Other Renal Tumors
12.1.2.1 Clear Cell Sarcoma of Kidney
12.1.2.2 Malignant Rhabdoid Tumor
12.1.2.3 Congenital Mesoblastic Nephroma
12.1.2.4 Renal Cell Carcinoma
12.1.3 Tumor Lysis Syndrome
12.1.3.1 Definition
12.1.3.2 Clinical Manifestations of TLS
12.1.3.3 Risk Factors for TLS
12.1.3.4 Mechanisms of AKI in TLS
12.1.3.5 General Principles of Management
12.1.3.6 Indications of Renal Replacement Therapy
12.1.3.7 Management of Electrolyte Abnormalities in TLS
12.2 Chemotherapy-Induced Renal Dysfunction
12.2.1 Risk Factors for Chemotherapy-Induced Renal Dysfunction
12.2.2 Sites of Renal Injury
12.2.3 Renal Toxicity of Selected Chemotherapeutic Drugs
12.2.4 Drugs Which Do Not Require Dose Modifications Based on Renal Dysfunction
12.3 Secondary Hypertension in the Oncology Setting
12.3.1 Tumors Associated with Hypertension
12.3.2 Mechanism of Hypertension
12.3.3 Evaluation of Hypertension
12.3.4 Management
12.4 Oligoanuria in the Oncology Setting
12.4.1 Prerenal Causes
12.4.2 Renal Causes
12.4.3 Postrenal Causes
12.4.4 Therapy
12.5 Renal Dysfunction and Stem Cell Transplantation
12.5.1 Overview of Stem Cell Transplantation (SCT)
12.5.2 The Steps of SCT
12.5.2.1 Conditioning
12.5.2.2 Stem Cell Infusion
12.5.2.3 Marrow Recovery
12.5.3 Renal Complications Following SCT
12.5.3.1 Acute Kidney Injury (AKI)
12.5.3.2 Chronic Kidney Disease
12.5.3.3 Nephrotic Syndrome
12.5.3.4 Renal Complications Associated with Sinusoidal Obstruction Syndrome (SOS)
12.5.4 Pretransplant Screening and Post-SCT Monitoring of Renal Status
Suggested Reading
13: The Kidney and the Tropics
13.1 Introduction
13.2 Classification
13.3 Malaria
13.4 Schistosomiasis
13.4.1 Schistosoma haematobium
13.4.2 Schistosoma mansoni
13.5 Filariasis
13.6 Onchocerciasis
13.7 Visceral Leishmaniasis (Kala-azar)
13.8 Leptospirosis
13.9 Rickettsial Infections
13.10 Enteric Pathogens
13.10.1 Salmonellosis
13.10.2 Yersinia Infections
13.10.3 Cholera
13.11 Renal and Genitourinary Tuberculosis
13.12 Viral Hemorrhagic Fevers
13.12.1 Dengue
13.12.2 Hantavirus
13.12.3 Yellow Fever
13.13 Snakebite Nephropathy
13.14 Scorpion Bite Nephropathy
13.15 Natural Medicines Causing Nephropathies
Conclusions
Suggested Reading
14: HIV and the Kidney
14.1 Introduction
14.2 Spectrum of HIV-Associated Renal Disease
14.2.1 HIV-Associated Nephropathy (HIVAN)
14.2.1.1 Introduction
14.2.1.2 Timeline
14.2.1.3 Pathogenesis
14.2.1.4 Genetic Aspects
14.2.1.5 Clinical Features
14.2.1.6 Ultrasonography
14.2.1.7 Unique Histological Findings
14.2.1.8 Treatment
14.2.2 Other HIV-Related Intrinsic Diseases of the Kidney
14.2.2.1 HIV-Associated Haemolytic Uremic Syndrome (HUS) and Thrombotic Microangiopathy
14.2.2.2 HIV-Associated Glomerulonephritis (GN)
14.2.2.3 Tubulopathy
14.2.3 Renal Manifestations of HIV Disease
14.2.4 Secondary Renal Effects
14.2.4.1 HIV-Associated Opportunistic Infections
14.2.4.2 Immune Reconstitution In ammatory Syndrome (IRIS)
14.2.4.3 Drug-Induced Nephropathy
14.3 Approach to a Child with HIV and Suspected Renal Disease
14.4 Dosing Adjustments for Antiretroviral Drugs in Chronic Kidney Disease
14.5 Renal Replacement Therapies in HIV-Infected Patients
14.5.1 Dialysis
14.5.2 Renal Replacement Therapies in HIV-Associated Renal Disease
14.6 Prognosis
Conclusion
Suggested Reading
15: Newborn and the Kidney
15.1 Introduction
15.2 Nephrogenesis
15.3 Foetal Origin of Adult Diseases (Barker's Hypothesis)
15.4 Amniotic Fluid
15.4.1 Oligohydramnios (Table 15.2)
15.4.2 Polyhydramnios (Table 15.3)
15.5 Perinatal Changes in Kidney Functions
15.5.1 Renal Blood Flow (RBF)
15.5.2 Glomerular Filtration Rate (GFR)
15.5.3 Urine Concentrating Capacity
15.5.4 Urine Diluting Capacity
15.5.5 Urine Output
15.5.6 Postnatal Changes in Distribution of Body Water
15.5.7 Vasoregulatory Mechanism of the Neonatal Kidney
15.5.8 Sodium
15.5.9 Potassium
15.5.10 Acid-Base Balance
15.5.11 Calcium and Phosphate
15.5.12 Uric Acid
15.5.13 Glucose
15.6 Assessment of Foetal Renal Functions
15.6.1 Foetal Glomerular Filtration Rate (GFR)
15.6.2 Foetal Urine
15.7 Clinical Practice
15.7.1 History
15.7.1.1 Family History
15.7.1.2 Antenatal History
15.7.2 Physical Examination
15.7.3 Extra-Renal Indicators for Newborn Renal Disease (Table 15.6)
15.7.4 Laboratory Evaluation
15.7.4.1 Urine Analysis
15.7.5 Assessment of Renal Functions
15.7.5.1 Serum Creatinine
Issues with Serum Creatinine as a Biomarker of Acute Kidney Injury
15.7.5.2 Other Markers
15.7.6 Radiological Examination
15.8 Fluids, Electrolytes and Acid-base Issues in the Newborn
15.8.1 Sodium
15.8.1.1 Hyponatremia
Signs and Symptoms of Hyponatremia
Management of Hyponatremia
15.8.1.2 Hypernatremia
Signs and Symptoms of Hypernatremia
Management of Hypernatremia
15.8.2 Potassium
15.8.3 Calcium
15.8.3.1 Osteopenia of Prematurity (Rickets)
15.8.4 Late Metabolic Acidosis
15.9 Acute Kidney Injury (Acute Renal Failure)
15.9.1 Classification of ARF
15.9.2 Incidence
15.9.3 Approach to ARF
15.9.3.1 History
15.9.3.2 Symptoms and Signs
15.9.4 Causes of ARF in Newborn (Table 15.10)
15.9.5 Some Neonatal Conditions Associated with Renal Failure
15.9.6 Diagnosis of ARF
15.9.7 Management of ARF
15.10 Neonatal Hypertension (Fig. 15.1)
15.10.1 Presentation
15.10.2 Measurement of BP
15.10.3 Investigations
15.10.4 Management
15.11 Nephrocalcinosis in the Premature Infant
15.12 Renal Vein Thrombosis (RVT)
Suggested Reading
16: Nephrotoxicity
16.1 Introduction
16.2 Endogenous Nephrotoxins
16.2.1 Hemoglobinuria
A Case Vignette
16.2.1.1 Causes of Hemoglobinuria
16.2.2 Myoglobinuria
A Case Vignette
16.2.2.1 Causes of Myoglobinuria
16.2.3 Clinical Presentation of Hemoglobinuria and Myoglobinuria (Pigment Nephropathy)
16.2.4 Pathophysiology of Pigment Nephropathy
16.2.5 Treatment of Pigment Nephropathy
16.2.6 Uric Acid Nephropathy
16.3 Exogenous Nephrotoxins
16.3.1 NSAIDs (Nonsteroidal Anti-in ammatory Drugs)
A Case Vignette
16.3.1.1 Acute Kidney Injury
16.3.2 Antibiotics
16.3.2.1 Aminoglycosides
16.3.2.2 Beta-Lactam Antibiotics
16.3.2.3 Glycopeptide Antibiotics (Vancomycin)
16.3.2.4 Others
16.3.3 Antifungals
16.3.3.1 Amphotericin B
16.3.4 Antivirals
16.3.4.1 Acyclovir and Ganciclovir
16.3.4.2 Other Antivirals
16.3.5 Chemotherapeutic Drugs
16.3.5.1 Cisplatin
16.3.5.2 Ifosfamide
16.3.5.3 Cyclophosphamide
16.3.5.4 Methotrexate
16.3.6 Calcineurin Inhibitors (Cyclosporine and Tacrolimus)
16.3.7 Angiotensin-Converting Enzyme (ACE) Inhibitors and Angiotensin Receptor-Blocking Agents (ARB)
16.3.8 Paracetamol
16.3.9 Radiocontrast Agents
16.3.9.1 Nephrogenic Systemic Fibrosis (NSF)
16.3.10 Miscellaneous
16.3.10.1 Herbal Medications
16.3.10.2 Ethylene Glycol and Methanol
16.3.10.3 Heavy Metals
16.3.10.4 Animal Toxins
16.3.10.5 Melamine Poisoning
Conclusions
Suggested Reading
17: Appendix
17.1 Normal Reference Values of Blood and Urine Chemistries
17.1.1 Blood Chemistries
17.1.2 Urine Chemistries
17.2 Conversion from Conventional Units to International Units (SI)
17.3 Important Drug Dosages
17.3.1 Antihypertensives
17.3.2 Diuretics
17.3.3 Immunosuppressants
17.3.4 Electrolyte Supplements
17.3.5 Phosphate Supplements
17.3.6 Calcium and Vitamin D Supplements
17.3.7 Miscellaneous Drugs
17.4 Drugs Dosages in Renal Failure
17.4.1 Antimicrobials Requiring Dosage Adjustments in Renal Failure
17.4.2 Non-antimicrobials requiring adjustments in renal failure
17.5 Diagnostic Protocols
17.5.1 Midstream Urine Collection
17.5.2 Suprapubic Aspiration (SPA)
17.5.2.1 Materials Required
17.5.2.2 Procedure
17.5.3 Per-Urethral Catheterization (PUC)
17.5.3.1 Indications
17.5.3.2 Materials Required
17.5.3.3 Procedure
17.5.3.4 Urinary Catheter Care
17.5.3.5 Complications
17.5.4 Clean Intermittent Catheterization (CIC)
17.5.5 Instructions for 24-h or a "Timed Urine Collection"
17.5.6 Instructions for a Split Urine Collection
17.6 Procedures
17.6.1 Voiding/Micturating Cystourethrogram (VCUG, MCUG)
17.6.1.1 Indications
17.6.1.2 Technique
17.6.2 Renal Biopsy
17.6.2.1 Prerequisites
17.6.2.2 Materials Required
17.6.2.3 Sedation
17.6.2.4 Procedure
17.6.2.5 Post-procedure Care
17.6.2.6 Complications
17.6.2.7 Contraindications
17.6.3 Plasma Exchange
17.6.3.1 Indications
17.6.3.2 Materials Required
17.6.3.3 Vascular Access
17.6.3.4 Procedure
17.6.3.5 Complications
17.6.4 Central Venous Access
17.6.4.1 Prerequisites
17.6.4.2 Equipment
17.6.4.3 Procedure (Seldinger Technique)
17.6.4.4 Insertion Site
Femoral Vein
Internal Jugular Vein (IJV)
Subclavian Vein
17.6.4.5 Complications of Central Venous Catheter Insertion
17.6.5 Acute Peritoneal dialysis
17.6.5.1 Materials Required
Peritoneal Dialysis Using Bicarbonate-Based PD Fluid
Indications
Composition and Preparation
Peritoneal Dialysis Using Chloride-Based PD Fluid
Indications
Composition
Dialysis
17.6.5.2 Procedure
17.6.5.3 Peritoneal Dialysis Prescription and Monitoring for Acute PD
17.6.5.4 Percutaneous Insertion of a Permanent Soft Catheter
Seldinger Technique
17.7 Nutritional Aspects
17.7.1 Maintenance Fluid Calculations by Body Weight
17.7.2 Recommended Calorie, Protein, Calcium, and Phosphorous Intake
17.7.3 Foods High in Sodium Content
17.7.4 Foods with High Levels of Potassium Content
17.7.5 Foods with Low Levels of Potassium Content
17.7.5.1 Reducing Potassium Levels in Vegetables
17.7.6 Foods High in Calcium Content
17.7.7 Foods High in Phosphate Content
17.7.8 Foods High in Oxalate Content
17.7.9 Dietary Guidelines for Obesity and Dyslipidemia
17.7.10 Total Parenteral Nutrition
17.8 Tools
17.8.1 Growth Charts: Weight, Height, BMI
17.8.1.1 CDC Charts
17.8.2 WHO Standards
17.8.2.1 Weight
17.8.2.2 Height
17.8.2.3 BMI
17.8.3 Surface Area Nomograms
17.8.4 Percentiles for Blood Pressure
17.8.5 Nomogram for Renal Length
Index

Inhalt (PDF)

Systemvoraussetzungen

Als PDF speichern Als Link merken

Manual of Pediatric Nephrology

Beschreibung

Rezensionen / Stimmen

Weitere Details

Weitere Ausgaben

Andere Ausgaben

Personen

Inhalt

Systemvoraussetzungen