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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •Preface
- •Malignant disease
- •Rheumatology
- •Water and electrolytes
- •Renal disease
- •Cardiovascular disease
- •Respiratory disease
- •Intensive care medicine
- •Poisoning, drug and alcohol abuse
- •Endocrinology
- •Diabetes mellitus and other disorders of metabolism
- •The special senses
- •Neurology
- •Dermatology
- •Elderly medicine and frailty
- •Abbreviations
- •Medical emergencies
- •Symptom Based
- •System Based
- •Infectious diseases and tropical medicine
- •Gastroenterology and nutrition
- •Liver, biliary tract and pancreatic disease
- •Diseases of the blood and haematological malignancies
- •Significant websites
- •Guidelines and evidence-based medicine
- •Medical calculators
- •Chapter-specific websites
- •Legally Valid Consent
- •Capacity
- •Information disclosure
- •Obtaining consent
- •Special circumstances
- •Adults who lack capacity to consent
- •Advance decisions
- •Children
- •Teaching
- •Human immunodeficiency virus testing
- •End-of-life decisions including assisted dying
- •Cardiopulmonary resuscitation
- •Confidentiality
- •Communication
- •The medical interview
- •1. Building a relationship
- •2. Opening the discussion
- •3. Gathering information
- •4. Understanding the patient
- •5. Sharing information
- •6. Reaching agreement on management
- •7. Providing closing
- •Breaking bad news
- •Communication in difficult circumstances
- •When things go wrong
- •Complaints
- •Culture and communication
- •Patients with impaired faculties for communication
- •Medical record keeping
- •Team communication
- •2 Infectious diseases
- •Common investigations in infectious disease
- •Septicaemia
- •Pyrexia of unknown origin
- •Investigations
- •Management
- •Common Viral Infections
- •Clinical features
- •Complications
- •Management
- •Clinical features
- •Management
- •Diagnosis
- •Management
- •Herpes viruses
- •Herpes simplex virus (HSV)
- •Investigations
- •Management
- •Varicella zoster virus
- •Varicella (chickenpox)
- •Herpes zoster (shingles)
- •Epstein–Barr virus infection
- •Clinical features
- •Investigations
- •Management
- •Bacterial Infections
- •Lyme disease
- •Clinical features
- •Investigations
- •Management
- •Clinical features
- •Investigations
- •Management
- •Rickettsia
- •Management
- •Treatment of uncomplicated falciparum malaria
- •Prevention and control
- •Clinical features
- •Investigations
- •Management and prevention
- •Enterocolitis
- •Dengue fever
- •Schistosomiasis
- •Fever in the Returned Traveller
- •Approach to diagnosis
- •Investigations
- •Aetiology
- •Pathogenesis
- •Clinical features
- •Investigations
- •Miscellaneous Viral Infections
- •Zika
- •MERS Co-V
- •Clostridium difficile
- •Pathology and clinical features
- •Management
- •Prevention of C. difficile infection
- •Travellers’ diarrhoea
- •Clinical features
- •Treatment and prevention
- •Clinical features
- •Intestinal amoebiasis (amoebic dysentery)
- •Amoebic liver abscess
- •Investigations
- •Serology
- •Colonic disease
- •Liver disease
- •Differential diagnosis
- •Management
- •Pathophysiology and clinical features
- •Management
- •Prevention and control
- •Giardiasis
- •Clinical features
- •Investigations
- •Management
- •Helminthic Infections
- •Sexually Transmitted Infections
- •Gonorrhoea
- •Clinical features
- •Diagnosis
- •Management
- •Chlamydia urethritis
- •Genital ulcers
- •Syphilis
- •Early stages
- •Primary infection
- •Secondary infection
- •Late stages
- •Tertiary syphilis
- •Congenital syphilis
- •Treponemal tests.
- •Non-treponemal tests.
- •Diagnosis
- •Management
- •Routes of acquisition
- •Pathogenesis of HIV infection
- •Natural history of HIV infection
- •Clinical features
- •Diagnosis
- •Human Immuodeficiency Virus
- •Monitoring
- •Management
- •Conditions due to immunodeficiency
- •Fungi
- •Protozoal infections
- •Viruses
- •Bacterial infection
- •Neoplasia
- •Prevention and control
- •Prognosis
- •Therapeutics
- •Antibacterials
- •β-Lactam antibacterials
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Cephalosporins
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Aminoglycosides
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Macrolides
- •Mechanism of action
- •Indications
- •Side effects
- •Metronidazole
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Quinolones
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Gastroenterology
- •Symptoms of Gastrointestinal Disease
- •Dyspepsia and indigestion
- •Dysphagia
- •Vomiting
- •Flatulence
- •Diarrhoea and constipation
- •Steatorrhoea
- •Abdominal pain
- •Investigation of Gastrointestinal Disease
- •Endoscopy
- •Oesophagogastroduodenoscopy (OGD, ‘gastroscopy’)
- •Sigmoidoscopy
- •Colonoscopy
- •Imaging
- •Plain X-rays
- •Ultrasound
- •Computed tomography (CT) scan
- •Magnetic resonance imaging (MRI)
- •Positron emission tomography (PET)
- •Contrast studies
- •Oesophageal physiology testing
- •The Mouth
- •Mouth ulcers
- •Non-infective
- •Infective
- •Oral white patches
- •The tongue
- •Periodontal disorders
- •Salivary gland disorders
- •The Oesophagus
- •Symptoms of oesophageal disorders
- •Gastro-oesophageal reflux disease (GORD)
- •Pathophysiology
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Peptic stricture
- •Barrett’s oesophagus
- •Achalasia
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Systemic sclerosis
- •Other oesophageal dysmotility disorders
- •Hiatus hernia
- •Benign oesophageal strictures
- •Oesophageal infection
- •Eosinophilic oesophagitis
- •Oesophageal perforation
- •Malignant oesophageal tumours
- •Pathology
- •Epidemiology and aetiological factors
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Benign oesophageal tumours
- •The Stomach and Duodenum
- •Helicobacter pylori infection
- •Epidemiology
- •Clinicopathological features
- •Diagnosis of infection
- •Management
- •Peptic ulcer disease
- •Epidemiology
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Management of dyspepsia
- •Gastropathy
- •Gastritis
- •Gastric cancer
- •Epidemiology
- •Aetiology
- •Pathology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Other gastric tumours
- •Gastrointestinal Bleeding
- •Acute upper gastrointestinal bleeding
- •Aetiology
- •Management
- •Endoscopy
- •Post-endoscopy
- •Lower gastrointestinal bleeding
- •Management
- •Chronic gastrointestinal bleeding
- •Investigations
- •Management
- •The Small Intestine
- •Coeliac disease (gluten-sensitive enteropathy)
- •Aetiology
- •Clinical features
- •Investigations
- •Other investigations
- •Management
- •Complications
- •Dermatitis herpetiformis
- •Tropical sprue
- •Bacterial overgrowth
- •Clinical features
- •Diagnosis
- •Management
- •Intestinal resection
- •Whipple’s disease
- •Miscellaneous Small Intestinal Conditions
- •Tuberculosis
- •Clinical features
- •Diagnosis
- •Management
- •Protein-losing enteropathy
- •Meckel’s diverticulum
- •Intestinal ischaemia
- •Tumours of the small intestine
- •Malignant tumours
- •Benign small bowel tumours
- •Carcinoid tumours
- •Pathology
- •Clinical features
- •Investigations
- •Management
- •Epidemiology
- •Aetiology
- •Genetic susceptibility
- •Environment
- •Inflammatory Bowel Disease
- •Host immune response
- •Pathology
- •Clinical features
- •Crohn’s disease
- •Ulcerative colitis
- •Radiology and imaging
- •Investigations
- •Differential diagnosis
- •Management
- •Medical
- •Induction of remission
- •Maintenance of remission
- •Surgery
- •Cancer in inflammatory bowel disease
- •Prognosis
- •Microscopic colitis
- •The Colon and Rectum
- •Constipation
- •Investigation
- •Management
- •Faecal incontinence
- •Diverticular disease
- •Aetiology
- •Clinical features
- •Management
- •Miscellaneous conditions
- •Megacolon
- •Ischaemic colitis
- •Adenomatous polyps
- •Colon polyps and the polyposis syndromes
- •Colorectal cancer
- •Epidemiology
- •Inheritance
- •Pathology
- •Clinical features
- •Investigation
- •Management
- •Prognosis
- •Screening
- •Diarrhoea
- •Mechanisms of diarrhoea
- •Osmotic diarrhoea
- •Secretory diarrhoea
- •Inflammatory diarrhoea (mucosal destruction)
- •Motility related
- •Approach to the patient with diarrhoea
- •Investigation
- •History
- •Examination
- •Investigations
- •Functional Bowel Disorders
- •The Acute Abdomen
- •Acute appendicitis
- •Epidemiology
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Complications
- •Acute peritonitis
- •Intestinal obstruction
- •The Peritoneum
- •Nutrition
- •Dietary requirements
- •Nutritional Support
- •Enteral nutrition
- •Total parenteral nutrition (TPN)
- •Monitoring of artificial nutrition
- •Refeeding syndrome
- •Disorders of BODY WEIGHT
- •Obesity
- •Anorexia nervosa
- •Therapeutics
- •Drugs for dyspepsia and peptic ulceration
- •Antacids
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •H2-receptor antagonists
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Proton pump inhibitors
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Constipation
- •Bulk-forming laxatives
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Stimulant laxatives
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Osmotic laxatives
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Bowel-cleansing solutions
- •Indications
- •Side effects
- •Diarrhoea
- •Side effects
- •Cautions/contraindications
- •Nausea and vomiting
- •Antihistamines
- •Indications
- •Mechanism of action
- •Side effects
- •Cautions/contraindications
- •Phenothiazines
- •Mechanism of action
- •Indications
- •Side effects
- •Domperidone and metoclopramide
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •5-HT3-receptor antagonists
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Liver Biochemistry and Liver Function Tests
- •Other Investigations in Liver and Biliary Disease
- •Symptoms and Signs of Liver Disease
- •Jaundice
- •Haemolytic jaundice
- •Congenital hyperbilirubinaemia
- •Cholestatic jaundice
- •Investigations
- •Hepatitis
- •Viral hepatitis
- •Hepatitis A
- •Epidemiology
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Prophylaxis
- •Hepatitis B
- •Epidemiology
- •Viral structure
- •Acute HBV infection
- •Chronic HBV infection
- •Treatment of chronic infection: who to treat
- •Antiviral agents
- •Hepatitis B and HIV co-infection
- •Prophylaxis
- •Hepatitis D (delta or δ agent)
- •Hepatitis C
- •Hepatitis C virus
- •Chronic hepatitis C infection
- •Hepatitis E
- •Acute hepatic failure
- •Alcohol use
- •Screening for problem drinking
- •Consequences of alcohol use and dependence
- •Autoimmune hepatitis
- •Aetiology
- •Clinical features
- •Investigations
- •Treatment
- •Prognosis
- •Aetiology
- •Pathology
- •Clinical features
- •Non-Alcoholic Fatty Liver Disease
- •Cirrhosis
- •Investigations
- •Severity
- •Aetiology
- •Further investigations
- •Management
- •Prognosis
- •Portal hypertension
- •Aetiology
- •Clinical features
- •Variceal haemorrhage
- •Management
- •Ascites
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Portosystemic encephalopathy
- •Pathophysiology
- •Clinical features
- •Differential diagnosis
- •Investigations
- •Management
- •Hepatorenal syndrome
- •Hepatopulmonary syndrome
- •Liver Transplantation
- •Types of Chronic Liver Disease and Cirrhosis
- •Alcoholic cirrhosis
- •Primary biliary cholangitis
- •Epidemiology
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Secondary biliary cirrhosis
- •Hereditary haemochromatosis
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Wilson’s disease (hepatolenticular degeneration)
- •α1-Antitrypsin deficiency
- •Alcohol and the liver
- •Fatty change
- •Alcoholic hepatitis
- •Clinical features
- •Investigations
- •Management
- •Alcoholic cirrhosis
- •Aetiology
- •Clinical features
- •Investigations
- •Treatment
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Primary Sclerosing Cholangitis
- •Budd–Chiari Syndrome
- •Liver Abscess
- •Liver Disease in Pregnancy
- •Liver Tumours
- •Hepatocellular carcinoma (hepatoma)
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Benign liver tumours
- •Pathophysiology
- •Clinical presentation
- •Gallstones
- •Biliary pain
- •Clinical features
- •Investigations
- •Management
- •Acute cholecystitis
- •Clinical features
- •Investigations
- •Management
- •Chronic cholecystitis
- •Acute cholangitis
- •Clinical features
- •Investigations
- •Management
- •Common bile duct stones (choledocholithiasis)
- •The Pancreas
- •Pancreatitis
- •Acute pancreatitis
- •Pathogenesis
- •Clinical features
- •Investigation
- •Management
- •General supportive care
- •Complications
- •Chronic pancreatitis
- •Clinical features
- •Investigations
- •Treatment
- •Epidemiology
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Carcinoma of the Pancreas
- •Cancer of the bile ducts
- •Neuroendocrine Tumours of the Pancreas
- •5 Haematological disease
- •Anaemia
- •Microcytic anaemia
- •Iron deficiency
- •Causes of iron deficiency
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Anaemia of chronic disease
- •Sideroblastic anaemia
- •Macrocytic anaemia
- •Megaloblastic anaemia
- •Vitamin B12 deficiency
- •Pernicious anaemia
- •Epidemiology
- •Clinical features
- •Investigation of vitamin B12 deficiency
- •Differential diagnosis
- •Management
- •Folate deficiency
- •Clinical features
- •Investigations
- •Management
- •Prevention of neural tube defects with folic acid.
- •Differential diagnosis
- •Anaemia caused by marrow failure (aplastic anaemia)
- •Aetiology
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Haemolytic Anaemia
- •Inherited Haemolytic Anaemias
- •Membrane defects
- •Hereditary spherocytosis
- •Clinical features
- •Investigations
- •Management
- •Hereditary elliptocytosis
- •Haemoglobin abnormalities
- •Thalassaemia
- •β-Thalassaemia
- •Investigations
- •Management
- •α-Thalassaemia
- •Sickle syndromes
- •Sickle cell anaemia
- •Clinical features
- •Vaso-occlusion.
- •Anaemia.
- •Long-term problems.
- •Investigations
- •Management
- •Red cell concentrates.
- •Platelet concentrates
- •Sickle cell trait
- •Metabolic red cell disorders
- •Glucose-6-phosphate dehydrogenase deficiency
- •Acquired Haemolytic Anaemia
- •Autoimmune haemolytic anaemia
- •‘Warm’ autoimmune haemolytic anaemia
- •Clinical features
- •Investigation
- •Management
- •‘Cold’ autoimmune haemolytic anaemia
- •Clinical features
- •Investigation
- •Management
- •Drug-induced haemolysis
- •Non-immune haemolytic anaemia
- •Paroxysmal nocturnal haemoglobinuria
- •Mechanical haemolytic anaemia
- •Myeloproliferative Disorders
- •Polycythaemia
- •Polycythaemia vera
- •Clinical features
- •Investigations
- •Management
- •Secondary polycythaemia
- •Essential thrombocythaemia
- •Myelofibrosis (myelosclerosis)
- •Clinical features
- •Investigations
- •Management
- •Myelodysplasia
- •The Spleen
- •Splenomegaly
- •Blood Transfusion
- •Fresh frozen plasma
- •Cryoprecipitate
- •Factor VIII and IX concentrates
- •Albumin
- •Immunoglobulins
- •Neutrophil leucocytosis
- •Neutropenia
- •Vascular/platelet bleeding
- •Coagulation disorders
- •Blood groups
- •Procedure for blood transfusion
- •Complications of transfusing red blood cells
- •The White Cell
- •Neutrophils
- •Eosinophils
- •Monocytes
- •Lymphocytes
- •Haemostasis and Thrombosis
- •Haemostasis
- •Investigation of bleeding disorders
- •Platelet disorders
- •Immune thrombocytopenic purpura (ITP)
- •Investigation
- •Management
- •First-line therapy.
- •Second-line therapy
- •Thrombotic thrombocytopenic purpura (TTP)
- •Inherited coagulation disorders
- •Haemophilia A
- •Clinical features
- •Investigations
- •Management
- •Complications
- •Haemophilia B (Christmas disease)
- •von Willebrand’s disease
- •Clinical features
- •Investigations
- •Management
- •Acquired coagulation disorders
- •Vitamin K deficiency
- •Disseminated intravascular coagulation (DIC)
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Liver disease
- •Thrombosis
- •Arterial thrombosis
- •Prevention
- •Treatment
- •Venous thrombosis
- •Prevention
- •Treatment
- •Treatment of established thromboembolism
- •Ferrous sulphate.
- •Folic acid.
- •Hydroxocobalamin.
- •Cyanocobalamin.
- •Phytomenadione.
- •Menadiol sodium phosphate
- •Aspirin.
- •Clopidogrel.
- •Therapeutics
- •Oral iron
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Folic acid
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Vitamin K
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Cautions/contraindications
- •Drugs affecting haemostasis
- •Antiplatelet agents
- •Mechanism of action
- •Indications
- •Side effects
- •Cautions/contraindications
- •Thrombin inhibitors
- •Mechanism of action
- •Indications
- •Warfarin.
- •Drug interactions.
- •Alteplase.
- •Side effects
- •Cautions/contraindications
- •Oral anticoagulants
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Contraindications
- •Direct oral anticoagulants (DOACs)
- •Mechanism of action
- •Preparations and indications
- •Side effects
- •Contraindications
- •Fibrinolytic drugs
- •Mechanism of action
- •Indications
- •Preparations and dose
- •Side effects
- •Contraindications
- •6 Malignant disease
- •Diagnosis of Malignancy
- •Cancer treatment
- •Chemotherapy
- •Radiotherapy
- •Endocrine therapy
- •Biological therapy
- •Myeloablative Therapy and Haemopoietic Stem Cell Transplantation (HSCT)
- •Oncological emergencies
- •The leukaemias
- •Aetiology
- •Acute leukaemia
- •Epidemiology
- •Clinical features
- •Investigations
- •Management
- •Treatment
- •Acute myeloid leukaemia
- •Acute promyelocytic leukaemia
- •Acute lymphoblastic leukaemia
- •Chronic myeloid leukaemia
- •Clinical features
- •Investigations
- •Management
- •Chronic lymphocytic leukaemia
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •The Lymphomas
- •Hodgkin’s lymphoma
- •Clinical features
- •Investigations
- •Differential diagnosis
- •Management
- •Non-Hodgkin’s lymphoma
- •Clinical features
- •Investigations
- •Management
- •The Paraproteinaemias
- •Multiple myeloma
- •Clinical features
- •Investigations
- •Management
- •Monoclonal gammopathy of undetermined significance
- •Management of pain
- •Palliation of nausea and vomiting
- •Care of the dying patient
- •Palliative Medicine and Symptom Control
- •7 Rheumatology
- •The Normal Joint
- •Musculoskeletal Symptoms
- •Common Investigations in Musculoskeletal Disease
- •Blood tests
- •Imaging
- •Synovial fluid analysis
- •Common Regional Musculoskeletal Problems
- •Back Pain
- •Lumbar back pain
- •Investigations
- •Management
- •Intervertebral Disc Disease
- •Acute disc disease
- •Clinical features
- •Investigations
- •Management
- •Chronic disc disease
- •Mechanical problems
- •Spondylolisthesis
- •Spinal stenosis
- •Neck pain
- •Epidemiology
- •Pathology and pathogenesis
- •Clinical features
- •Differential diagnosis
- •Investigations
- •Management
- •Osteoarthritis
- •Inflammatory Arthritis
- •Rheumatoid arthritis
- •Epidemiology
- •Aetiology and pathogenesis
- •Pathology
- •Clinical features
- •Non-articular manifestations
- •Investigations
- •Differential diagnosis
- •Management
- •Prognosis
- •The Seronegative Spondyloarthritis
- •Axial spondylarthritis
- •Clinical features
- •Investigations
- •Management
- •Psoriatic arthritis
- •Clinical features
- •Investigations
- •Treatment
- •Reactive arthritis
- •Clinical features
- •Investigations
- •Management
- •Enteropathic arthritis
- •Crystal Arthritis
- •Gout and hyperuricaemia
- •Epidemiology
- •Pathogenesis
- •Clinical features
- •Investigations
- •Management
- •Pseudogout (pyrophosphate arthropathy)
- •Investigations
- •Management
- •Infection of Bones and Joints
- •Septic arthritis
- •Clinical features
- •Management
- •Specific types of bacterial arthritis
- •Osteomyelitis
- •Autoimmune Rheumatic Diseases
- •Systemic lupus erythematosus
- •Epidemiology
- •Aetiology
- •Pathogenesis
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Antiphospholipid syndrome
- •Clinical features
- •Management
- •Systemic sclerosis (scleroderma)
- •Aetiology
- •Clinical features
- •Limited cutaneous scleroderma (LcSSc, 70% of cases)
- •Diffuse cutaneous scleroderma (DcSSc, 30% of cases)
- •Investigations
- •Management
- •Prognosis
- •Polymyositis and dermatomyositis
- •Clinical features
- •Investigations
- •Management
- •Sjögren’s syndrome
- •Clinical features
- •Investigations
- •Management
- •‘Overlap’ syndrome and undifferentiated autoimmune rheumatic disease
- •Systemic Inflammatory Vasculitis
- •Polymyalgia rheumatica and giant cell arteritis
- •Clinical features
- •Investigations
- •Management
- •Takayasu’s arteritis
- •Polyarteritis nodosa
- •Kawasaki disease
- •Microscopic polyarteritis (polyangiitis)
- •Eosinophilic granulomatosis with polyangiitis
- •Henoch–Schönlein purpura
- •Cryoglobulinaemic vasculitis
- •Behçet’s disease
- •Diseases of Bone
- •Control of calcium and bone metabolism
- •Vitamin D
- •Parathyroid hormone
- •Osteoporosis
- •Aetiology
- •Clinical features
- •Investigations
- •Assessment of fracture risk
- •Management
- •Clinical features
- •Investigations
- •Treatment
- •Osteomalacia and vitamin D deficiency
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Therapeutics
- •Anti-inflammatories and pain relief
- •Paracetamol (acetaminophen)
- •Non-steroidal anti-inflammatory drugs
- •Mechanism of action
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Gastrointestinal toxicity.
- •Other side effects
- •Cautions/contraindications
- •Drugs affecting bone metabolism
- •Bisphosphonates
- •Mechanism of action
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Calcium
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Vitamin D
- •Mechanism of action
- •Indications
- •Examples of preparations and doses
- •Side effects
- •Water and Electrolyte Requirements
- •Body Fluid Compartments
- •Distribution of extracellular fluid
- •Glucocorticoid-induced osteoporosis
- •Osteonecrosis
- •Paget’s disease
- •Aetiology
- •Intravenous fluids in clinical practice
- •Regulation of Body Fluid Homeostasis
- •Regulation of extracellular volume
- •Abnormalities of extracellular volume
- •Increased extracellular volume
- •Clinical features
- •Aetiology
- •Management
- •Decreased extracellular volume
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Plasma Osmolality and Disorders of Sodium Regulation
- •Regulation of body water content
- •Hyponatraemia
- •Hyponatraemia resulting from salt loss (hypovolaemic hyponatraemia)
- •Clinical features
- •Management
- •Hyponatraemia resulting from water excess (dilutional hyponatraemia)
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Central pontine myelinolysis
- •Hypernatraemia
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Disorders of Potassium Regulation
- •Hypokalaemia
- •Aetiology
- •Clinical features
- •Management
- •Hyperkalaemia
- •Aetiology
- •Clinical features
- •Management
- •Disorders of Magnesium Regulation
- •Hypomagnesaemia
- •Aetiology
- •Clinical features
- •Management
- •Hypermagnesaemia
- •Disorders of Acid–Base Balance
- •Respiratory acidosis
- •Respiratory alkalosis
- •Metabolic acidosis
- •Clinical features
- •Differential diagnosis (the anion gap)
- •Lactic acidosis
- •Diabetic ketoacidosis
- •Renal tubular acidosis
- •Uraemic acidosis
- •Metabolic alkalosis
- •Clinical features
- •Management
- •Therapeutics
- •Diuretics
- •Thiazide diuretics
- •Examples
- •Mechanism of action
- •Indications
- •Side effects
- •Loop diuretics
- •Examples
- •Mechanism of action
- •Indications
- •Side effects
- •Potassium-sparing diuretics and aldosterone antagonists
- •Examples
- •Mechanism of action
- •Indications
- •Side effects
- •9 Renal disease
- •Presenting Features Of Renal Disease
- •Dysuria
- •Polyuria and nocturia
- •Oliguria
- •Haematuria
- •Pain
- •Investigation Of Renal Disease
- •Blood tests
- •Glomerular filtration rate
- •Urine dipstick testing
- •Proteinuria
- •Haematuria
- •Glycosuria
- •Urine microscopy
- •White cells
- •Red cells
- •Casts
- •Bacteria
- •Imaging techniques
- •Transcutaneous renal biopsy
- •Glomerular Diseases
- •Normal glomerular structure
- •Pathogenesis and terms in glomerular disease
- •Classification and presentation of glomerulopathies
- •Aetiology
- •Nephrotic syndrome with ‘bland’ urine sediments
- •Nephrotic syndrome with ‘active’ urine sediments (mixed nephrotic/nephritic)
- •Clinical features
- •Differential diagnoses
- •Investigations
- •Management
- •General oedema
- •Specific treatment
- •Complications
- •Nephrotic Syndrome
- •Acute glomerulonephritis (acute nephritic syndrome)
- •Clinical features
- •Investigations
- •Management
- •Rapidly progressive glomerulonephritis
- •Urinary Tract Infection
- •Pathogenesis
- •Risk factors for UTI
- •Clinical features
- •Natural history
- •Investigations
- •Diagnosis
- •Treatment of single isolated attack
- •Recurrent infection.
- •Management
- •UTI in pregnancy
- •Abacteriuric frequency or dysuria (‘urethral syndrome’)
- •Bacterial prostatitis
- •Tuberculosis of the urinary tract
- •Tubulointerstitial Nephritis
- •Acute tubulointerstitial nephritis
- •Chronic tubulointerstitial nephritis
- •Hypertension and the Kidney
- •Essential hypertension
- •Renal hypertension
- •Bilateral renal disease
- •Renovascular disease
- •Options for renal artery imaging
- •Management
- •Aetiology
- •Calcium stones
- •Uric acid stones
- •Infection-induced stones
- •Cystine stones
- •Clinical features
- •Differential diagnosis
- •Investigations
- •Management
- •Renal Calculi and Nephrocalcinosis
- •Nephrocalcinosis
- •Aetiology
- •Clinical features
- •Investigations
- •Management
- •Epidemiology
- •Clinical and biochemical features
- •Urinary Tract Obstruction
- •Acute Kidney Injury
- •Investigation of the uraemic emergency
- •Investigations
- •Management
- •Prognosis
- •Aetiology
- •Chronic Kidney Disease
- •Clinical features and investigations
- •Differentiating AKI from CKD
- •Management
- •Renoprotection
- •Reduce cardiovascular risk
- •Correction of complications
- •Referral to a nephrologist
- •Renal Replacement Therapy
- •Dialysis
- •Haemodialysis
- •Peritoneal dialysis
- •Haemofiltration
- •Complications of all long-term dialysis
- •Transplantation
- •Cystic Renal Disease
- •Solitary and multiple renal cysts
- •Autosomal-dominant polycystic kidney disease
- •Clinical features
- •Diagnosis
- •Management
- •Medullary sponge kidney
- •Tumours of the Kidney and Genitourinary Tract
- •Renal cell carcinoma
- •Clinical features
- •Investigations
- •Management
- •Prognosis
- •Urothelial tumours
- •Clinical features
- •Investigations
- •Management
- •Diseases Of The Prostate Gland
- •Benign enlargement of the prostate gland
- •Clinical features
- •Investigations
- •Management
- •Prostatic carcinoma
- •Clinical features
- •Investigation
- •Management
- •Screening
- •Clinical features
- •Investigations
- •Treatment
- •Testicular Tumour
- •Urinary Incontinence
- •Normal bladder physiology
- •Stress incontinence
- •Urge incontinence
- •Overflow incontinence
- •Neurological causes
- •Chest pain
- •Dyspnoea
- •Palpitations
- •Syncope
- •Other symptoms
- •Investigations in Cardiac Disease
- •The chest X-ray
- •ECG waveform and definitions (Fig. 10.5)
- •The Electrocardiogram
- •Exercise electrocardiography
- •24-hour ambulatory taped electrocardiography
- •Tilt testing
- •Echocardiography
- •Cardiac nuclear imaging
- •Cardiac computed tomography
- •Cardiovascular magnetic resonance
- •Positron emission tomography
- •Cardiac catheterization
- •Cardiac Arrhythmias
- •General principles of management of arrhythmias
- •Sinus rhythms
- •Sinus arrhythmia
- •Bradycardias and heart block
- •Sinus bradycardia
- •Neurally mediated syndromes
- •Heart block
- •Atrioventricular block
- •Bundle branch block
- •Supraventricular tachycardias
- •Sinus tachycardia
- •Atrioventricular junctional tachycardias
- •Atrioventricular nodal re-entry tachycardia (AVNRT)
- •Atrioventricular reciprocating tachycardia (AVRT)
- •Symptoms
- •Acute management
- •Long-term management
- •Atrial tachyarrhythmias
- •Atrial fibrillation
- •Management
- •Assessment for anticoagulation
- •Atrial flutter
- •Ventricular tachyarrhythmias
- •Ventricular ectopic premature beats (extrasystoles)
- •Sustained ventricular tachycardia
- •Non-sustained ventricular tachycardia
- •Ventricular fibrillation
- •Long QT syndrome
- •Cardiac arrest
- •Aetiology
- •Pathophysiology
- •Venous return (preload)
- •Outflow resistance (afterload)
- •Myocardial contractility
- •Neurohormonal and sympathetic system activation: salt and water retention
- •Natriuretic peptides
- •Antidiuretic hormone (vasopressin)
- •Clinical features
- •Symptoms
- •Signs
- •Investigations
- •Treatment of chronic heart failure
- •Heart Failure
- •Drug treatment
- •Non-pharmacological treatment
- •Acute heart failure
- •Clinical features
- •Management
- •Irreversible risk factors for coronary artery disease
- •Potentially changeable risk factors
- •Estimation of cardiovascular risk
- •Ischaemic Heart Disease
- •Angina
- •Clinical features
- •Diagnosis
- •Investigations
- •Management
- •Acute coronary syndromes
- •Clinical features
- •Treatment of NSTEMI and unstable angina
- •Risk stratification
- •ST segment elevation myocardial infarction (STEMI)
- •Clinical features
- •Investigations
- •Management
- •Complications (Table 10.10)
- •Disturbances of rate, rhythm and conduction (p. 411)
- •Post-ACS drug therapy and assessment
- •Epidemiology
- •Clinical features
- •Investigations
- •Treatment
- •Rheumatic Fever
- •Chronic rheumatic heart disease
- •Valvular Heart Disease
- •Prosthetic heart valves
- •Mitral stenosis
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Mitral regurgitation
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Prolapsing (‘floppy’) mitral valve
- •Aetiology
- •Clinical features
- •Investigation
- •Management
- •Aortic stenosis
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Aortic regurgitation
- •Aetiology
- •Pathophysiology
- •Symptoms
- •Signs
- •Investigations
- •Management
- •Tricuspid and pulmonary valve disease
- •Infective endocarditis
- •Aetiology
- •Pathology
- •Clinical features
- •Investigations
- •Diagnostic criteria
- •Management
- •Surgery
- •Pulmonary Heart Disease
- •Pulmonary hypertension
- •Aetiology

Therapeutics 343
therapy or hyperaldosteronism. Vomiting causes alkalosis, both by causing
volume depletion and through loss of gastric acid.
Clinical features
Cerebral dysfunction is an early feature of alkalosis. Respiration may be
depressed.
Management
This includes fluid replacement, if necessary, with replacement of sodium,
potassium and chloride. The bicarbonate excess will correct itself.
THERAPEUTICS
Diuretics
Diuretics (see Table 8.4) reduce sodium and chloride reabsorption at different
sites in the nephron and thus increase urinary sodium and water loss.
Thiazide diuretics
Examples
Bendroflumethiazide, metolazone.
Mechanism of action
They inhibit sodium reabsorption at the beginning of the distal convoluted
tubule and reduce peripheral vascular resistance.
Indications
In low doses, they are used to reduce blood pressure; at higher doses, to
relieve oedema in patients with mild chronic heart failure and good renal
function.
Side effects
Postural hypotension, anorexia, diarrhoea, metabolic and electrolyte disturbances (hyponatraemia, hypokalaemia, hypomagnesaemia, hypercalcaemia,
hyperuricaemia and gout). May aggravate diabetes mellitus.
Loop diuretics
Examples
Furosemide, bumetanide.
Mechanism of action
Loop diuretics stimulate excretion of sodium chloride and water by blocking
the sodium–potassium–chloride channel in the thick ascending limb of the
loop of Henle. Loop diuretics also increase venous capacitance and thus

344 Water, electrolytes and acid–base balance
produce rapid clinical improvement before the diuresis in patients with acute
heart failure.
Indications
Loop diuretics are given intravenously in patients with acute pulmonary
oedema due to left heart failure. They are administered orally in patients
with chronic heart failure and in patients with oedema associated with liver
disease if aldosterone antagonists alone are ineffective. High doses may be
needed with impaired renal function.
Side effects
Metabolic disturbance (hypokalaemia, hypomagnesaemia, hyponatraemia,
hyperuricaemia causing gout, hyperglycaemia) tinnitus and deafness with
rapid i.v. administration or high doses.
Potassium-sparing diuretics and aldosterone antagonists
Examples
Spironolactone, amiloride.
Mechanism of action
Potassium-sparing diuretics and aldosterone antagonists inhibit sodium
reabsorption in the cortical collecting tubule. Amiloride and triamterene
directly decrease sodium channel activity; spironolactone inhibits aldosterone. They have weak natriuretic activity.
Indications
Spironolactone is used in ascites and oedema associated with chronic liver
disease and in low doses to improve survival in severe heart failure. Amiloride
in combination with loop diuretics can be used as an alternative to giving
potassium supplements. Amiloride may be used in patients with liver disease
who are intolerant of spironolactone because of gynaecomastia.
Side effects
Hyperkalaemia, gynaecomastia, acute kidney injury.

9
The kidneys are 11–14 cm in length and lie retroperitoneally on either side of
the vertebral column from T12–L3. The functions of the kidneys are:
• Elimination of waste material
• Regulation of volume and composition of body fluid
• Endocrine function – production of erythropoietin, renin and vitamin D in
its active form
• Autocrine function – production of endothelin, prostaglandins, renal
natriuretic peptide.
The functional unit of the kidney is the nephron, of which there are about
1 million in each kidney. Each nephron is composed of a glomerulus, proximal
tubule, loop of Henle, distal tubule and collecting duct (Fig. 9.1). The renal
artery (a branch of the abdominal aorta) supplies the kidney and divides many
times to form afferent arterioles, which supply the glomerular capillary tuft
before draining into efferent arterioles. Efferent arterioles from (outer) cortical
glomeruli drain into a peritubular capillary network within the renal cortex and
then into increasingly larger branches of the renal vein. By contrast, blood
from the (inner) juxtamedullary glomeruli passes via vasa recta in the medulla
and returns via the cortex to renal veins that drain into the inferior vena cava.
The wider diameter of the afferent compared to efferent arterioles increases
the pressure of blood within the glomerulus and forces water and solutes
(but not red blood cells or larger molecular weight plasma proteins) out of
the glomerular capillaries into the Bowman’s capsule, forming the glomerular
filtrate (about 170–180 L per day). The proximal renal tubules reabsorb most
of the filtered solute required to maintain fluid and electrolyte balance, but
elimination of potassium, water and non-volatile hydrogen ions is regulated in
the distal tubules. As renal perfusion and glomerular filtration fall, reabsorption
of water and sodium by the proximal tubules increases so that minimal fluid
reaches the distal tubule. Hence, hypotensive or hypovolaemic patients
cannot excrete potassium and hydrogen ions. Patients with distal tubular
damage, e.g. caused by drugs, also cannot excrete potassium and hydrogen
ions. Normally only about 1% of the original filtered volume, containing high
concentrations of urea and creatinine, passes into the renal pelvis as urine.
Renal disease
PRESENTING FEATURES OF RENAL DISEASE
The most common diseases of the kidney and urinary tract are benign
prostatic hypertrophy in men and urinary tract infections (UTIs) in women.

346 Renal disease
Filtered blood
Afferent
Glomerulus (‘capillary bed’=
Loop of Henle
Waste products
(urine)
to the bladder
Fig. 9.1 The kidney and a nephron.
Renal vein draining
to inferior vena cava
Blood with waste
products
Renal artery
Ureter
arteriole
network of blood capillaries)
Efferent arteriole
Bowman’s capsule
Proximal convoluted
tubule (PCT)
Renal cortex
Renal medulla
Descending
limb of Henle
Vasa
recta
Distal convoluted
tubule (DCT)
Collecting duct
(leading to the
pelvis of the
kidney, also
known as the
‘renal pelvis’)
Ascending
limb of Henle

Presenting Features of Renal Disease 347
Symptoms suggesting renal tract disease are dysuria, frequency of micturition, haematuria, urinary retention and alteration of urine volume (either
polyuria or oliguria). In addition there may be pain anywhere along the renal
tract, from loin to groin. Non-specific symptoms, e.g. lethargy, anorexia and
pruritus, may be the presenting features of chronic kidney disease (CKD).
Renal disease may be asymptomatic and discovered by an incidental finding
of hypertension, a raised serum urea, or proteinuria and haematuria on urine
dipstick testing.
Dysuria
Dysuria (pain on micturition) is caused by:
• Inflammation involving the urethra (urethritis) or bladder (cystitis). Dysuria
is common in adult women and is usually due to lower urinary tract
bacterial infection (p. 362). Other causes of urethritis include infection
with Chlamydia trachomatis or Neisseria gonorrhoeae (pp. 45–46).
• Inflammation involving the vagina in women or glans penis in men.
Causes include infection with Candida albicans and Gardnerella vaginalis.
Polyuria and nocturia
Polyuria is an excessive urine output of greater than 2.5–3 L in 24 hours.
It must be differentiated from the more common complaints of urinary
frequency and nocturia (night-time urination), which are not necessarily
associated with an increase in the total urine output. Causes of polyuria
include polydipsia (defined as excessive thirst leading to increased fluid
intake >3 L per day), solute diuresis (e.g. hyperglycaemia with glycosuria),
diabetes insipidus and CKD. Nocturia is most often due to drinking before bed
or, in men over 50 years, prostatic enlargement (p. 394).
Oliguria
Oliguria describes a low urine output. If maintained over several hours this
indicates acute kidney injury (AKI, p. 375) or urinary tract obstruction. It may
be ‘physiological’, as in patients with hypotension and hypovolaemia, where
urine is maximally concentrated in an attempt to conserve water. Anuria (no
urine) suggests bilateral ureteric or bladder outflow obstruction. Management
of the oliguric patient involves three steps:
1. Exclude obstruction. The patient with outflow obstruction (acute urinary
retention) is typically in great discomfort with an intense desire to
micturate. The bladder is palpable as a tender mass arising out of the
pelvis that is dull to percussion. The diagnosis is confirmed by passing a

348 Renal disease
urethral catheter and releasing a large volume of urine. If the patient is
already catheterized, the catheter should be flushed with sterile saline to
relieve any blockage. Obstruction proximal to the bladder (e.g. ureteric
obstruction) is often painless. Ultrasound examination is indicated to
exclude pelvicalyceal dilatation.
2. Assess for hypovolaemia. Once obstruction has been excluded,
the patient should be assessed for evidence of hypovolaemia by
measurement of blood pressure, pulse, jugular venous pressure (JVP)
and urinary electrolytes (p. 349). If the patient is hypovolaemic, the urine
output in response to a fluid challenge is assessed.
3. Management of established AKI. (p. 380) Once obstruction and
hypovolaemia have been excluded, management should focus
on treating the AKI and correcting any underlying cause where
appropriate.
Haematuria
See urine dipstick testing (p. 351).
Pain
Loin/flank pain occurs in kidney infections (acute pyelonephritis), upper
urinary tract obstruction and occlusion of the renal artery due to either thrombosis in situ or emboli. Chronic renal pain occurs in cystic renal disease and
renal tumours. Acute severe pain radiating from the flank to the iliac fossa
and testes or labium is typical of ureteric colic due to a calculus.
INVESTIGATION OF RENAL DISEASE
Once renal disease is suspected, the purpose of investigation is to determine the cause and the presence or degree of renal dysfunction. The
estimated glomerular filtration rate (eGFR, see below) is used to determine
the degree of renal dysfunction. The history and examination together with
urine dipstick testing and microscopy of urine are the starting points for
diagnosis.
Blood tests
The serum urea or creatinine concentration represents the dynamic equilibrium between production and elimination but levels do not rise above
the normal range until there is a reduction of 50%–60% in the glomerular
filtration rate (GFR). The serum urea concentration may be increased by
a high-protein diet, increased tissue catabolism (surgery, trauma, infection), and gastrointestinal bleeding, whereas the level of creatinine is less

Investigation of Renal Disease 349
()
()
dependent on diet but more related to age, gender and muscle mass. Once
elevated, serum creatinine is a better guide to GFR than urea, although a
normal level is not synonymous with a normal GFR.
Glomerular filtration rate
Measurement of the GFR is the best indicator of kidney function. Daily
production of creatinine (primarily from muscle cells) is fairly constant and
generally unaffected by protein intake. Serum creatinine and excreted (urinary) creatinine vary little throughout the day, allowing measurement of the
creatinine clearance. It is calculated using a 24-hour urine collection and
a single plasma creatinine. However, measurement of GFR is cumbersome
and time-consuming, and may be inaccurate if 24-hour urine collections
are incomplete. Several formulae have been developed to predict creatinine
clearance or GFR based on serum creatinine and patient characteristics
including age, weight, gender and ethnicity (e.g. the Cockroft–Gault equation,
the modification of diet in renal disease (MDRD) equation and the CKDepidemiology (CKD-EPI) collaboration equation).
Calculation of creatinine clearance using the
Cockroft–Gault equation
Men
Creatinine clearance
Women. Use the same equation but multiply by 1.04 instead of 1.23.
These equations have not been fully validated across all ranges of renal
impairment, weights or body mass index (BMI), or in all ethnic groups.
However, for monitoring patients with acute or chronic kidney disease, the
convenience and ease of the eGFR has led to its widespread adoption.
1.23 140 AgeWeight in kg
=
−
××()
Serum cr
eeatininemol /L
µ
Urine dipstick testing
Urine dipstick testing detects the presence of blood, protein, glucose,
ketones, bilirubin and urobilinogen in the urine and provides a semiquantitative assessment of the amount of substance present. Dipsticks can also be
used to measure urine pH, which is useful in the investigation and management of renal tubular acidosis (p. 343). Each test is based on a colour change
in a strip of absorbent cellulose impregnated with the appropriate reagent.
The stick is dipped briefly into a fresh specimen of urine collected in a clean
container and the colour changes compared with the manufacturer’s colour
charts on the reagent strip container. Haematuria or proteinuria suggests
renal tract disease. Dipsticks are also available for testing for urinary nitrites
and leucocyte elastase to identify UTIs (p. 362).

350 Renal disease
Proteinuria
This is an excess of protein in the urine. Under normal conditions the low
molecular weight proteins and albumin that are filtered by the glomerulus
are almost completely reabsorbed in the proximal renal tubule. This results
in a normal urinary protein excretion of less than 150 mg/day, of which only
a small amount is albumin (<30 mg daily). Dipsticks are albumin specific
and will detect albumin once urine levels exceed 200 mg/L (300 mg daily if
urine volume is normal). Dipsticks do not detect abnormal proteins such as
globulins and Bence Jones protein (immunoglobulin light chains) excreted
in multiple myeloma. The causes of proteinuria are listed in Table 9.1.
Persistent proteinuria detected on dipstick testing requires full investigation
and should be quantified. Quantification of proteinuria is by measurement
of protein and/or albumin concentration in a ‘spot’ urine sample (ideally an
early morning specimen) and normalizing to creatinine concentration to give
a urine protein-to-creatinine ratio (PCR) or the more sensitive urine albuminto-creatinine ratio (ACR). Normal protein excretion is less than 150 mg per
day (PCR <15 mg/mmol) and nephrotic range proteinuria (p. 357) is more
than 3.5 g per day (PCR >350 mg/mmol).
Table 9.1 Causes of proteinuria
Type Mechanism Examples
Glomerular Increased permeability Glomerulopathies
Tubular*
Overflow
Decreased reabsorption
Plasma proteins produced in
excess
Physiological
†
Increased renal
haemodynamics
*Usually <1 g per day and may be associated with other defects of proximal tubular
function (e.g. glucosuria, phosphaturia, aminoaciduria).
†Mild proteinuria and not associated with underlying renal disease. Diagnosis is made
by the absence of proteinuria on subsequent urine examinations when the condition, e.g.
fever, resolves.
Fanconi’s syndrome
Tubulointerstitial
disorders
Multiple myeloma
Monoclonal gammopathy
Acute illness
Fever
Intense activity
Upright posture

Investigation of Renal Disease 351
Infarct
Stone
Stone
Parasites
Tubulointerstitial
nephritis
Papillary
necrosis
Tumour
Ureteric neoplasms
Bleeding disorders
Microalbuminuria is an increase above the normal range in urinary
albumin excretion that is undetectable by conventional dipsticks (i.e.
30–300 mg/day). It is an early indicator of renal disease and is widely used
as a predictor of the development of nephropathy in people with diabetes.
An ACR of >2.5 mg/mmol in men and >3.5 mg/mmol in women indicates
microalbuminuria. Albumin excretion above 300 mg/day is overt proteinuria.
Haematuria
Haematuria is blood in the urine and is either visible (macroscopic or gross)
or non-visible (microscopic).
Haematuria can arise from several sites in the kidney or urinary tract
(Fig. 9.2).
• Blood that is only apparent at the start of micturition is usually due to
urethral disease
• Blood at the end of micturition suggests bleeding from the prostate or
bladder base
• Blood seen as an even discoloration throughout the urine suggests
bleeding from a source in the bladder or above.
Trauma
Cysts
Tuberculosis
Glomerulonephritis
Single
Multiple
Urethra
Trauma
Infection
Fig. 9.2 Sites and causes of bleeding from the urinary tract.
Carcinoma
or stones
Carcinoma or
papilloma
Infection
Prostate
Benign hypertrophy
Carcinoma

352 Renal disease
Haematuria
Exclude transient causes
Visible haematuria Non-visible haematuria
Plasma Cr for eGFR
Urology assessment
Renal tract imaging
+ cystoscopy
Fig. 9.3 Decision algorithm for the investigation of haematuria. Cr, creatinine; eGFR,
estimated glomerular filtration rate; ACR (PCR), albumin (protein):creatinine ratio.
Plasma Cr for eGFR
Urine for ACR or PCR
Age 40 years or
Symptomatic
Normal
investigations
Repeat yearly Nephrology referral
All
others
Abnormal
investigations
Fig. 9.3 outlines an algorithm for the investigation of haematuria. Patients
should be evaluated regardless of anticoagulant or antiplatelet therapy.
Transient causes such as urinary tract infection and contamination during
menstruation should be excluded by repeat testing. Urinary tract malignancy is
more likely in patients with visible haematuria, urinary tract symptoms or those
over 40 years of age. Urological referral should be considered for appropriate
imaging of the urinary tract (either ultrasound or computed tomography [CT])
and cystoscopy. All other patients are more likely to have glomerular disease
(often immunoglobulin [Ig]A nephropathy) and nephrology referral is indicated
if initial or subsequent testing of renal function is abnormal.
Glycosuria
Diabetes mellitus must be excluded in any patients with a positive dipstick
test for glucose.
Urine microscopy
This is performed on a fresh, clean-catch, mid-stream urine specimen in all
patients suspected of having renal disease.
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