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The Resource Acute Nephrology for the Critical Care Physician

Acute Nephrology for the Critical Care Physician

Label
Acute Nephrology for the Critical Care Physician
Title
Acute Nephrology for the Critical Care Physician
Creator
Contributor
Subject
Language
eng
Summary
This practical guide provides the reader with answers to important clinically relevant questions regarding the evaluation and management of acute kidney injury (AKI). All aspects of critical care nephrology are covered, from pathophysiology and diagnosis to prevention and treatment. The questions considered relate to a wide range of issues, such as: How do I diagnose AKI? How can I protect the kidney in clinical practice? How do I manage patients with AKI? When should I initiate and how do I perform renal replacement therapy (RTT)? Which type of RTT is most appropriate for my patient? Should I give specific nutrients? In addition to providing practical guidelines and treatment algorithms, the book includes calculators for continuous RRT and anticoagulant dosing. The authors are internationally renowned experts in the fields of Intensive Care Medicine and Nephrology and all contributions are written in a clear and concise style and have been peer reviewed. Acute Nephrology for the Critical Care Physician will serve as a very useful source for intensivist internists, anesthesiologists and nephrologists involved in the management and treatment of critically ill patients at risk of or affected by AKI
Cataloging source
MiAaPQ
Literary form
non fiction
Nature of contents
dictionaries
Acute Nephrology for the Critical Care Physician
Label
Acute Nephrology for the Critical Care Physician
Link
http://libproxy.rpi.edu/login?url=https://ebookcentral.proquest.com/lib/rpi/detail.action?docID=2094724
Publication
Copyright
Related Contributor
Related Location
Related Agents
Related Authorities
Related Subjects
Carrier category
online resource
Carrier category code
cr
Carrier MARC source
rdacarrier
Color
multicolored
Content category
text
Content type code
txt
Content type MARC source
rdacontent
Contents
  • Preface -- Contents -- Part I: Acute Kidney Injury -- 1: AKI: Definitions and Clinical Context -- 1.1 Acute Kidney Injury -- 1.1.1 AKI Definitions -- 1.2 Comorbidities and the Risk of AKI -- 1.2.1 Susceptibility -- 1.2.2 Exposures -- 1.2.3 AKI Risk Assessment -- Conclusion -- References -- 2: Epidemiology of AKI -- 2.1 Incidence of AKI -- 2.1.1 Population-Based Incidence -- 2.1.2 Proportion of AKI Patients -- 2.2 Risk Factors Associated with AKI -- 2.2.1 Predisposing Factors/Chronic Diseases -- 2.2.2 Acute Diseases/Drugs -- 2.3 Outcomes of AKI Patients -- 2.3.1 Hospital Mortality -- 2.3.2 Long-Term Fixed-Time Mortality (90 Days, 6 Months) -- 2.3.3 Trends in Mortality -- 2.3.4 Factors Associated with Mortality -- 2.3.5 Health-Related Quality of Life (HRQoL) of AKI Survivors -- 2.4 Summary -- References -- 3: Renal Outcomes After Acute Kidney Injury -- 3.1 Introduction -- 3.2 AKI and the Development of CKD -- 3.2.1 Epidemiology of CKD After AKI -- 3.2.2 Pathophysiology of CKD After AKI -- 3.3 Diagnosis of CKD in AKI Survivors -- 3.4 Primary Prevention of CKD After AKI -- 3.5 Managing CKD After AKI -- 3.5.1 Proposed Follow-Up Pathway After AKI -- Conclusion -- References -- 4: Etiology and Pathophysiology of Acute Kidney Injury -- 4.1 Introduction -- 4.2 Sepsis -- 4.2.1 Renal Hemodynamics in Sepsis -- 4.2.2 Regulation of Renal Hemodynamics in Sepsis -- 4.2.3 Cell Signaling and Inflammation -- 4.2.4 Tissue Injury and Apoptosis -- 4.3 Ischemia and Reperfusion (I/R) -- 4.3.1 Hemodynamics -- 4.3.2 Endothelial and Vascular Smooth Muscle Injury -- 4.3.3 Tubular Injury -- 4.3.4 Cell Signaling and Inflammation -- 4.3.5 Tissue Apoptosis, Necrosis, and Repair -- 4.4 Nephrotoxicity -- 4.4.1 Agents Altering Hemodynamics -- 4.4.2 Agents Causing Injury to Small Vessels -- 4.4.3 Agents Causing Glomerular Injury
  • 4.4.4 Agents Causing Tubular Injury -- 4.4.5 Agents Causing Injury by Urinary Obstruction -- 4.4.6 Agents Causing Injury to the Interstitium -- Conclusions -- References -- 5: Acid-Base -- 5.1 Introduction -- 5.2 The Stewart Approach -- 5.2.1 Strong Ion Difference (SID) -- 5.2.2 Total Amount of Weak Acids (ATOT) -- 5.2.3 The Partial Pressure of Carbon Dioxide (PCO2) -- 5.2.4 Strong Ion Gap (SIG) and Urine SID -- 5.2.5 Osmol Gap -- 5.2.6 Effect of Resuscitation Fluids -- 5.3 The Henderson-Hasselbalch Approach -- 5.3.1 Anion Gap and Urine Anion Gap -- 5.3.2 Delta Ratio -- 5.4 Base Excess and Standard Base Excess -- 5.5 Stewart at the Bedside: A Unifying Approach -- 5.6 When and How to Treat Acid-Base Disorders -- 5.7 Renal Acid-Base Handling -- 5.7.1 Renal Tubular Acidosis (RTA) -- 5.7.2 Acute Kidney Injury (AKI) -- 5.7.3 Chronic Kidney Disease (CKD) -- 5.7.4 Renal Replacement Therapy (RRT) -- Conclusion -- Further Reading -- 6: Kidney-Organ Interaction -- 6.1 Introduction -- 6.2 The Kidney and the Heart -- 6.2.1 Type I Cardiorenal Syndrome -- 6.2.2 Type III Cardiorenal Syndrome -- 6.3 The Kidney and the Lung -- 6.3.1 Impact of AKI on Lung Function -- 6.3.2 Impact of Lung Injury on the Kidney -- 6.4 The Kidney in the Abdominal Compartment -- 6.4.1 Intra-abdominal Hypertension and Abdominal Compartment Syndrome -- 6.4.2 Elevated Intra-abdominal Pressure and Renal Function -- 6.4.3 Gut Microbiota and the Intestinal Barrier Function -- 6.4.4 Hepatorenal Syndrome -- 6.4.5 Conclusions -- 6.5 The Kidney and the Brain -- 6.5.1 Hyponatremia -- 6.5.2 Hypernatremia -- 6.5.3 Acute Kidney Injury and the Brain -- 6.5.4 Conditions Affecting Both the Kidney and Brain -- Conclusions -- References -- 7: Acute Kidney Injury in Pregnancy -- 7.1 Introduction -- 7.2 Epidemiology -- 7.3 Physiological Changes in Pregnancy
  • 7.4 Laboratory Testing -- 7.5 Pathophysiology -- 7.5.1 First Trimester -- 7.5.2 Second and Third Trimester -- 7.5.2.1 Preeclampsia and Hemolysis, Elevated Liver Enzymes, and Low Platelets (HELLP) Syndrome -- 7.5.2.2 Thrombotic Microangiopathies -- 7.5.2.3 Acute Fatty Liver of Pregnancy -- 7.5.2.4 Renal Cortical Necrosis -- 7.5.2.5 Infectious Complications Contributing to AKI during Pregnancy -- Urinary Tract Infections -- Sepsis/Multiple Organ Failure -- 7.5.2.6 Urinary Tract Obstruction and Nephrolithiasis -- 7.6 Prevention -- References -- Part II: Diagnosis of AKI -- 8: Classical Biochemical Work Up of the Patient with Suspected AKI -- 8.1 Introduction -- 8.2 Biochemical Work Up -- 8.2.1 Creatinine and the Assessment of Renal Function -- 8.2.2 Clearance Measurements -- 8.2.3 Alternatives to Creatinine: Cystatin C and Urea -- 8.2.4 Mathematical Estimation of GFR -- 8.3 Urinalysis in AKI -- 8.3.1 Urine Analysis -- 8.3.2 Urine Microscopy -- 8.4 Urine Chemistry -- 8.4.1 Urinary Sodium -- 8.4.2 Fractional Excretion of Sodium (FeNa) -- 8.4.3 Fractional Excretion of Urea (FeU) -- 8.5 Non-biochemical Investigations and Renal Biopsy in AKI -- 8.5.1 Further Investigations -- 8.5.2 Serological Testing and Biopsy -- 8.6 Oliguria in AKI -- References -- 9: Acute Kidney Injury Biomarkers -- 9.1 Introduction -- 9.2 Types of Biomarkers -- 9.3 Novel AKI Biomarkers in Clinical Practice -- 9.3.1 Diagnosis of Early AKI -- 9.3.1.1 Subclinical AKI -- 9.3.1.2 In the Emergency Department -- 9.3.1.3 Post-cardiac Surgery -- 9.3.1.4 During Critical Illness -- 9.3.2 Prediction of Outcome in AKI -- 9.3.2.1 Need for RRT -- 9.3.2.2 Renal Recovery -- 9.3.2.3 Prediction of Mortality -- 9.3.3 Prediction of Renal Function After Transplantation -- 9.4 Adjunctive Roles -- 9.5 Unmet Needs -- References
  • 10: Renal Imaging in Acute Kidney Injury -- 10.1 Renal Echography -- 10.1.1 Brightness Mode (B-Mode) -- 10.1.2 Doppler-Based Resistive Index (RI) -- 10.1.2.1 Methods -- 10.1.2.2 Normal Values, Feasibility and Reproducibility -- 10.1.2.3 Significance and Usual Confounders -- 10.1.2.4 Clinical Relevancy in ICU -- 10.1.3 Contrast-Enhanced Ultrasonography -- 10.2 Computerized Tomography -- 10.3 Magnetic Resonance Imaging -- Conclusion -- References -- Part III: Prevention and Protection -- 11: Prevention of AKI and Protection of the Kidney -- 11.1 Introduction -- 11.2 Ensuring Adequate Kidney Perfusion -- 11.2.1 Optimizing Systemic Hemodynamics -- 11.2.1.1 Vasopressors -- 11.2.1.2 Inotropes -- 11.2.1.3 Volume Therapy -- 11.2.2 Reducing Factors Compromising Renal Perfusion -- 11.2.3 Selective Renal vasodilation -- 11.2.3.1 Dopamine -- 11.2.3.2 Prostaglandins -- 11.2.3.3 Natriuretic Peptide -- 11.3 Modulation of Renal Physiology -- 11.3.1 Renal Metabolism, Tubular Obstruction -- 11.3.2 Oxygen Radical Damage -- 11.3.2.1 N-acetylcysteine -- 11.3.2.2 Mannitol -- 11.3.2.3 Selenium -- 11.3.2.4 Ascorbic Acid -- 11.3.3 Avoiding Additional Nephrotoxic Damage -- 11.3.3.1 Aminoglycoside -- 11.3.3.2 Amphotericin B -- 11.3.3.3 Angiotensin-Converting Enzyme Inhibitors -- References -- Part IV: Renal Replacement Therapy -- 12: Timing of Renal Replacement Therapy -- 12.1 Introduction -- 12.2 Triggers for Starting RRT -- 12.3 Literature Review -- 12.4 Current Clinical Practice Guideline Recommendations -- 12.5 Discontinuation of RRT in the ICU -- 12.6 Future Clinical Trials -- 12.7 Conclusions: Decision Making on Starting RRT at the Bedside -- References -- 13: Dose of Renal Replacement Therapy in AKI -- 13.1 Introduction -- 13.2 Prescription of Dose of RRT -- 13.3 Dose Intensity of RRT in AKI and Outcome -- 13.4 Fluid Overload and RRT
  • 13.5 High-Volume Hemofiltration in Septic Shock -- 13.6 Risks of "Too Little" and "Too Much" RRT -- References -- 14: Type of Renal Replacement Therapy -- 14.1 Principles of Diffusion and Convection -- 14.2 Types of Renal Replacement Therapy for AKI: Intermittent versus Continuous -- 14.2.1 Intermittent Techniques -- 14.2.2 Continuous Therapies -- 14.2.3 Continuous versus Intermittent Therapies -- 14.3 'Hybrid' Technologies: Prolonged Intermittent Renal Replacement Therapy for AKI -- 14.4 Postdilution versus Predilution -- 14.4.1 Postdilution -- 14.4.2 Predilution -- References -- 15: Anticoagulation for Continuous Renal Replacement Therapy -- 15.1 Heparin Anticoagulation for Continuous Venovenous Hemofiltration (CRRT) -- 15.2 Heparin Induced Thrombocytopenia -- 15.3 Prostacyclin -- 15.3.1 Indication -- 15.3.2 Practical Considerations -- 15.3.3 Alone or Incombination with Heparin -- 15.3.4 Dose and Side Effects -- 15.4 Citrate Anticoagulation for Continuous Renal Replacement Therapy -- 15.4.1 Summary -- 15.4.2 Introduction -- 15.4.3 Regional Anticoagulation -- 15.4.4 Citrate Is a Buffer -- 15.4.5 Principles of the Citrate Circuit -- 15.4.6 Modalities -- 15.4.7 Monitoring of Citrate Anticoagulation -- 15.4.8 Citrate Accumulation -- 15.4.9 Benefits of Citrate Anticoagulation -- 15.5 CRRT Without Anticoagulation -- 15.6 Non-anticoagulant Measures to Maximize Hemofilter Survival -- References -- 16: Metabolic Aspects of CRRT -- 16.1 Acidosis -- 16.1.1 Summary -- 16.2 Electrolyte Management During CRRT -- 16.2.1 Summary -- 16.2.2 Introduction -- 16.2.3 Potassium and Phosphate -- 16.2.4 Role of Effluent Volume -- 16.2.5 Intermittent Versus Continuous -- 16.2.6 Calcium -- 16.2.7 Magnesium -- 16.2.8 Monitoring of Electrolytes During CRRT -- 16.3 Nutrition and Micronutrients -- 16.3.1 Summary
  • 16.3.2 General Recommendations
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unknown
http://library.link/vocab/discovery_link
{'f': 'http://opac.lib.rpi.edu/record=b4383056'}
Extent
1 online resource (280 pages)
Form of item
online
Isbn
9783319173894
Media category
computer
Media MARC source
rdamedia
Media type code
c
Sound
unknown sound
Specific material designation
remote

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