Presentations
- Acidosis
- Haematuria
- Hypertension
- Hypertensive emergency
- Fluid overload
- Oligo-anuria
- Oliguria
- Proteinuria
- Sodium, potassium, and calcium disturbances
- Uraemia
Conditions
- Nephrotoxins
- Outflow obstruction
- Sepsis
- Reduced perfusion
For each presentation and condition, Advanced Trainees will know how to:
Synthesise
- recognise the clinical presentation
- identify relevant epidemiology, prevalence, pathophysiology, and clinical science
- take a relevant clinical history
- conduct an appropriate examination
- establish a differential diagnosis
- plan and arrange appropriate investigations consider the impact of illness and disease on patients19 and their quality of life
Manage
- provide evidence-based management
For less common or more complex presentations and conditions the trainee must also seek expert opinions
- prescribe therapies tailored to patients’ needs and conditions
- recognise potential complications of disease and its management, and initiate preventative strategies
- involve multidisciplinary teams
Consider other factors
- identify individual and social factors and the impact of these on diagnosis and management
Conditions
- Abdominal compartment syndromes
- Atypical haemolytic uraemic syndrome/thrombotic microangiopathy (TMA)
- Cardio-renal syndromes Congenital anomalies of kidney and urinary tract (CAKUT)
- Delayed graft function post-kidney transplant
- Endemic nephropathy
- Haematology disorders, including monoclonal gammopathy of renal significance (MGRS) (AIM only)
- Hepato-renal syndrome
- Infections of the urinary tract and kidney
- Renal artery dissection:
- toxicological indications for dialysis drug metabolism, pharmacokinetics in patients with reduced kidney function
- Renal-vascular disease:
- Rhabdomyolysis and myoglobinuric AKI
- Tumour lysis syndrome
For each presentation and condition, Advanced Trainees will know how to:
Synthesise
- recognise the clinical presentation
- identify relevant epidemiology, prevalence, pathophysiology, and clinical science
- take a relevant clinical history
- conduct an appropriate examination
- establish a differential diagnosis
- plan and arrange appropriate investigations consider the impact of illness and disease on patients19 and their quality of life
Manage
- provide evidence-based management
For less common or more complex presentations and conditions the trainee must also seek expert opinions
- prescribe therapies tailored to patients’ needs and conditions
- recognise potential complications of disease and its management, and initiate preventative strategies
- involve multidisciplinary teams
Consider other factors
- identify individual and social factors and the impact of these on diagnosis and management
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Pathophysiology of acute tubular injury
- Hypoxia
- Inflammatory response
- Linkages between physiology and pathophysiology
- Normal physiology – AKI, tubular abnormalities, metabolic acidosis, drug induced acidosis, sodium
- Tubular factors:
- proximal tubular injury including apoptosis and necrosis
- sub-lethal proximal tubular injury
- Vascular factors:
Investigations
- ADAMTS-13
- Clinical diagnosis versus biochemical versus biomarkers
- Contemporary biomarkers (blood and urine) of AKI
- Current biomarkers for research
- Full blood count (FBC)
- Immunology testing, including:
- antineutrophil cytoplasmic antibodies (ANCA)
- anti-glomerular basement membrane (anti GBM)
- antinuclear antibodies (ANA)
- Anti-DNase B
- creatine kinase (CK)
- complement component 3 (C3)
- complement component 4 (C4)
- cryoglobulins
- double stranded NDA (dsDNA)
- extractable nuclear antigen (ENA)
- serum electrophoresis (light and heavy) chain
- KDIGO stages G1–G5
- Kidney histopathology
- MRI
- Nuclear medicine scans
- Peripheral blood (PB) film (aHUS/TMA)
- Arterio-venous fistulas of the kidney post biopsy
- Stool for ST-producing E. coli (STEC)
- Ultrasound or CT of kidneys, ureters, and bladder (KUB)
- Urine microscopy
- Urine albuminuria/proteinuria
- Urine electrolytes (stone work-up)
- AKI following endovascular procedures
- Haptoglobin and lactate dehydrogenase (LDH) to full blood count for haemolytic uremic syndrome (HUS)
- Difficult management issues
- Acidaemia
- Appropriate fluid prescription
- Disequilibrium
- Electrolyte and acid base disturbances
- High AKI risk groups in the emergency department, including:
- cardiac arrest
- CKD
- heart failure
- hyponatraemia
- increased creatinine
- liver disease
- myocardial infarction
- post-trauma
- sepsis
- shock
- toxic ingestions
- Hyperkalaemia
- Malignant hypertension or emergent hypertension
- Uraemia
- Vascular access complications:
- bleeding
- central line-associated bloodstream infections (CLABSI)
- pneumothorax
- Nephrotoxicity of medications/drugs and therapies
- Antibiotics
- Anti-fungal agents
- Anti-inflammatories
- Iodinated contrast (intra-arterial)
- Nephrotoxic agents, such as:
- checkpoint inhibitors
- cisplatin
- proto-inhibitors
- Some herbal supplements and natural therapies
- Toxic alcohols – ethylene glycol, methanol
- Vascular endothelial growth factor inhibitors
- Pregnancy
- Causes of AKI in pregnancy
- Comorbid medical conditions in patients with pre-existing kidney disease, dialysis, or a kidney transplant during pregnancy, with particular emphasis on risk minimisation
- Hypertension
- Nephrotic syndrome in pregnancy
- Pre-eclampsia and eclampsia
- Prescribing, therapy, and pharmacology
- Choice of kidney replacement therapy modality, intensity of solute and volume removal, anticoagulation
- Choice of vascular access
- Dialysis and drug metabolism
- Plasmapheresis or plasma exchange
- Timing of initiating acute kidney replacement therapy
- Urgent indications for acute kidney replacement therapy
-
Prevention
- Primary prevention in high-risk patients (e.g. cardiac surgery)
- Secondary prevention in patients at risk of recurrent AKI
PCH
- Choice of modality for acute kidney replacement therapy
- Definitions and staging of AKI in children and neonates
- Fluid status evaluation
- Diarrhoea-associated (D+) haemolytic uremic syndrome and diarrhoea negative (D-) or atypical HUS, and use of biologics
- Prevention and management of AKI in neonates
