Renal Failure and Replacement Therapies (eBook)

Table of Contents 6
Contributors 8
1 Assessment of Renal Function 9
Normal Functions of the Kidney 9
The Role of the Kidney in Homeostasis 9
Body Fluid Composition 9
Clinical Evaluation of Renal Function 9
Urea 10
Creatinine 10
Assessment of GFR 11
Estimated Ca: The Cockroft and Gault Formula (2) 11
Urinalysis (4, 5) 11
Appearance 11
Specific Gravity 11
Volume 11
Chemical Testing 12
Blood 12
Protein 12
Glucose 13
Bacteriuria 13
Urine Microscopy 13
White Blood Cells 13
Red Blood Cells 14
Casts 14
References 14
Suggested Reading 14
2 Imaging of Acute Renal Failure—A Problem-Solving Approach for Intensive Care Unit Physicians 15
Acute or Chronic Renal Failure? 15
Acute Tubular Necrosis 15
Glomerulonephritis and Acute Interstitial Nephritis 17
Ureteric Obstruction 17
Renal Artery Dissection or Occlusion 18
Renal Vein Thrombosis 19
Renal Artery Stenosis 21
Conclusion 21
References 21
3 Drug-Induced Renal Injury 22
Risk Factors for Nephrotoxicity 22
Methods of Prevention 22
Nonsteroidal Anti-Inflammatory Drugs 22
Effects on Renal Prostaglandins 22
Other Renal Effects 23
ACEIs and ARBs 24
Aminoglycosides 24
Contrast Nephropathy 24
Incidence and Outcome 24
Methods of Prevention 25
Intravenous Hydration 25
N-Acetylcysteine 25
Type of Contrast Used 25
Other Therapies (18, 19) 25
Suggestions for High-Risk Patients 25
References 25
4 Acute Kidney Injury 27
Definition of AKI 27
Incidence and Outcome 27
Causes of AKI 28
Prerenal Failure 28
Intrinsic Renal Failure 28
Postrenal or Obstructive Renal Failure 30
Complications of AKI 30
Retention of Uremic Toxins 30
Volume Overload 30
Acidosis 30
Electrolyte and Mineral Disturbances 30
Anemia 30
Immunosuppression 30
Metabolic Consequences 30
Drug Accumulation 30
Investigation of the Cause of Renal Failure (Table 4.1) 31
Laboratory Tests (Table 4.2) 31
Urinalysis 31
Radiological Investigations 31
Conclusion 31
References 32
5 Medical Management of Acute Renal Failure 34
Diagnosis of ARF 34
Investigations 34
Assessment of Renal Function 34
Urinalysis 34
Other Markers of Renal Injury 35
Radiology 35
Renal Biopsy 35
Primary Prevention 35
Loop Diuretics 35
Mannitol 36
Dopamine Agonists 36
N-Acetylcysteine 36
Others 36
Supportive Strategies 36
Postinjury Prevention of ARF 37
Assessment and Correction of Volume Depletion 37
Maintenance of Adequate MAP and Cardiac Output 37
Avoidance of Further Insults 37
Renal Replacement Therapy 37
Summary 38
References 38
6 Acute Renal Failure in the Surgical Patient 41
Pathophysiology of ARF 41
Risk Factors for ARF in the Surgical Patient (Table 6.1) 41
Effect of Anesthesia 41
Effect of Drugs 41
Development of Intra-abdominal Compartment Syndrome 42
Type of Surgery 42
Cardiac Surgery (Table 6.2) 42
Methods of Prevention of ARF 42
Vascular Surgery 43
Urological Surgery 43
Diagnosis (Table 6.3) 43
Treatment 43
General Measures 43
Specific Measures 44
Treatments that Have Not Been Shown to Alter the Course of ARF 44
Vasopressor Agents and the Kidney 44
Prevention 44
General Vigilance 44
Early Resuscitation 44
Prevention of Contrast-Induced Nephropathy 44
Tight Glucose Control 44
Prophylactic Dopamine or Diuretics 44
Natriuretic Peptides 44
Future Advances 45
References 45
7 Rhabdomyolysis and Compartment Syndrome 46
Causes 46
Compartment Syndrome 46
Diagnosis 46
Creatine Kinase 46
Hyperkalemia 46
Acidosis 47
Early Hypocalcemia and Late Hypercalcemia 47
Hyperphosphatemia 47
Urinary Abnormalities 47
Pathophysiology of ARF 47
Treatment 48
Intravascular Volume Expansion 48
Alkalinization 48
Mannitol 48
Dialysis/Hemofiltration 48
Prognosis 48
Summary 48
Suggested Reading 49
8 Multisystem Causes of Acute Renal Failure 50
Systemic Vasculitis 50
Etiology 50
Presentation 50
Symptoms 50
Signs 50
Laboratory Investigations (Table 8.3) 51
Imaging 51
Renal Biopsy 51
Treatment 51
Resuscitation 51
Maintenance 52
Disease-Specific Treatment 52
Outcome 52
Systemic Lupus Erythematosus 53
Laboratory Testing 53
Imaging 54
Treatment 54
Thrombotic Microangiopathy 54
Etiology 54
Presentation 54
Differential Diagnosis 54
Laboratory Investigations 55
Treatment and Outcome 55
References 55
9 Therapeutic Plasma Exchange 57
Indications (Table 9.2) 57
Prescription (Table 9.1) 57
After Procedure 57
Complications 58
10 Renal Replacement Therapy 59
The Basics 59
Classification of RRT 60
Duration or Timing of Therapy 60
Access 60
Mechanism of Solute Removal 60
Intensity of Therapy 61
Indications for RRT 61
“Traditional” indications (19) 61
“Nonrenal” Indications 61
Choosing the Dose and Mode of RRT 62
Summary 63
References 63
11 Technical Aspects of Renal Replacement Therapy 65
Mode of CRRT 65
Hemofiltration Machines (Figure 11.2) 67
Replacement and Dialysis Fluid 67
Prefilter Versus Postfilter Infusion 68
Lactate Versus Bicarbonate Buffer 68
Hemofilters 68
Structure 68
Membrane Characteristics 68
Biocompatibility 68
Flux 68
Vascular Access 68
Positioning 69
Site of Catheter 69
Anticoagulation 69
No Anticoagulation 69
Unfractionated Heparin 69
Low Molecular Weight Heparin 70
Regional Citrate Anticoagulation 70
Prostacyclin 71
Other Anticoagulants 71
Comment 71
References 71
Suggested Reading 71
12 End-Stage Renal Disease 72
Hemodialysis and Peritoneal Dialysis 72
Mechanisms of Dialysis 72
Hemodialysis 72
Peritoneal Dialysis 72
Clinical Parameters 73
Dialysis-Related Complications 75
Hemodialysis 75
Peritoneal Dialysis 75
Renal Transplantation 75
Evaluation, Selection, and Preparation of the Potential Transplant Recipient 76
General Evaluation 76
Psychological Evaluation 76
Recurrent Renal Disease 76
Immunological 76
Evaluation and Selection of Donors 76
Immunosuppression 76
Complications of Transplantation 77
Immediate 77
Early 77
Late 77
Summary 78
References 78
Suggested Reading 78
13 Clinical Hyperkalemia and Hypokalemia 79
Hyperkalemia 79
Causes of Hyperkalemia 79
Compartmental Shift 79
Decreased Renal Excretion 79
Clinical Features 79
Electrocardiogram Changes 79
Pseudohyperkalemia 80
Management 81
Stabilization of Cardiac Membranes: Intravenous Calcium 81
Transcellular Redistribution 81
Removal of Excess Potassium 81
Hypokalemia 81
Causes of Hypokalemia (Table 13.3) 82
Familial Hypokalemic Periodic Paralysis 82
Magnesium Depletion 83
Clinical Effects 83
Neuromuscular 83
Mild Hypokalemia 83
Moderate Hypokalemia 83
Severe Hypokalemia 83
Cardiovascular 83
Arrhythmias 83
ECG Changes 83
Worsening of Cardiac Function 83
Renal and Metabolic 83
Ammoniagenesis and Metabolic Alkalosis 83
Nephrogenic Diabetes Insipidus 84
Diagnostic Approach to Hypokalemia 84
Treatment 84
Suggested Reading 84
14 Clinical Hyponatremia and Hypernatremia 85
Hyponatremia 85
Classification (Table 14.1) 85
Pseudohyponatremia 85
Transurethral Resection of the Prostate (TURP) Syndrome 85
Syndrome of Inappropriate Antidiuretic Hormone Secretion 85
Clinical Presentation 87
Diagnosis 87
Treatment 87
Asymptomatic Patients 87
Symptomatic Patients 87
Hypernatremia 87
Classification (Table 14.3) 87
Mechanism 88
Clinical Presentation 88
Evaluation of Hypernatremia 88
Interpretation of Urinary Osmolality 88
Treatment 88
15 Clinical Metabolic Acidosis and Alkalosis 89
Traditional Versus Physiochemical Approach to Acid-Base Disturbances 89
Lactic Acidosis (Table 15.4) 91
Use of Sodium Bicarbonate 91
Use of Renal Replacement Therapy 92
Metabolic Alkalosis 92
Initiating Processes 93
Perpetuating Factors 93
Treatment 93
References 93
Index 95

"8 Multisystem Causes of Acute Renal Failure (p. 42-43)

Tim Leach

This chapter covers some of the more specialized causes of acute renal failure, which, although more likely to present to the nephrologist, could be admitted to the intensive care unit as a consequence of their illness or because of complications of their treatment.

Systemic Vasculitis

Vasculitis is the term given to in? ammation of blood vessels. Vasculitis is a rare condition, with an incidence of approximately 6 people per million (Western) population per year (1). Vessels can be classi? ed according to their size (Table 8.1) (2). Renal failure can occur in any vasculitis, but this chapter focuses on those conditions that affect renal function directly through in? ammation within the glomeruli (small vessels), rather than affecting the kidneys indirectly through a reduction of blood supply to the kidneys (large and medium vessel diseases).

Etiology

Small vessel vasculitides separate into two broad groups: those in which immune complexes are deposited within the renal glomeruli and those without evidence of deposition histologically. The latter group are termed pauci-immune; lacking (literally “few”) immune complexes. This distinction is useful for making a histological diagnosis and for estimating prognosis, but the underlying cause of these small vessel vasculitides is similar: autoimmunity.

Normally, the immune system surveys cells and tissues within the body, recognizing and ignoring cells expressing “self” antigens while attacking cells without these protective epitopes. In autoimmune conditions, the immune system does not protect cells with “self” expression. Cells are attacked and either in? amed or killed, or circulat- ing self-antigens are bound with antibody-forming immune complexes. Immune complexes are very large molecules that are often unable to pass through capillaries because of their size. They can induce local in? ammation and activate the com- plement cascade.

Presentation Symptoms Renal failure as a result of fulminant small vessel vasculitis will present acutely, and patients may be systemically unwell, requiring organ support. More often, however, there is an indolent presentation with several months of nonspeci? c symptoms and signs (Table 8.2).

Signs

Fulminant systemic vasculitis presents with the nephritic syndrome:
• Azotemia (more often with oligoanuria)
• Hypertension and edema from ? uid overload (but can present with circulatory collapse caused by vasodilation and dehydration)
• Hematuria with red cell casts
"