S10) Acute Kidney Injury Flashcards
What is acute kidney injury?
- AKI is a clinical syndrome wherein there is an abrupt decline in actual GFR (days to weeks)
- This disrupts homeostasis (ECF volume, electrolyte and acid-base) and leads to an accumulation of nitrogenous waste products
In terms of laboratory findings, provide three definitions of AKI
- Increase in serum creatinine by ≥ 26.5 μmol/L within 48 hours
- Increase in serum creatinine by ≥1.5 times baseline within 7 days
- Urine volume <0.5 ml/kg/h for 6 hours
Define Stage 1 AKI in terms of serum creatinine and urine output
- Serum Cr criteria: ↑ Cr ≥ 150-200% from baseline
- Urine output criteria: <0.5 mL/kg/hr for >6 h
Define Stage 2 AKI in terms of serum creatinine and urine output
- Serum Cr criteria: ↑ Cr > 200-300% from baseline
- Urine output criteria: <0.5 mL/kg/h for >12 h
Define Stage 3 AKI in terms of serum creatinine and urine output
- Serum Cr criteria: ↑ Cr >300% from baseline or initiated on RRT
- Urine output criteria: <0.3 mL/kg/h for 24 h or anuria for 12 h
Identify the three causes of AKI
- Pre-renal failure (volume responsive)
- Intrinsic renal failure
- Post-renal failure
Describe the epidemiology of AKI in high income countries in terms of:
- Typical patients
- Location
- Causes
- Treatment
- Patients: older people
- Location: hospital-acquired AKI
- Causes: dehydration and hypotension
- Treatment: dialysis withheld most commonly due to futility
Describe the epidemiology of AKI in low income countries in terms of:
- Typical patients
- Location
- Causes
- Treatment
- Patients: younger people (often children)
- Location: community-acquired AKI
- Causes: dehydration, hypotension, obstetric causes, snake and insect bites
- Treatment: dialysis withheld due to lack of resources
In 6 steps, outline the pathophysiology of pre-renal AKI
⇒ Decreased renal blood flow
⇒ Reduced actual GFR
⇒ Kidneys work hard to restore blood flow (no cell damage)
⇒ Reabsorb Na+ & H2O (aldosterone, ADH release)
⇒ If mild hypoperfusion, autoregulation preserves renal blood flow
⇒ If overwhelmed compensatory responses, AKI occurs
Explain how prescription drugs can affect renal perfusion
- NSAIDS and ACEi can override intrinsic autoregulatory mechanisms
- Disease of the afferent arteriole (BP, DM) can result in too great or too little a response to these stimuli
Describe the causes of pre-renal AKI in terms of:
- Reduced effect arterial blood volume
- Impaired renal autoregulation
- Reduced effective arterial blood volume:
I. Hypovolaemia
II. Systemic vasodilation – sepsis, cirrhosis, anaphylaxis
III. Cardiac failure
- Impaired renal autoregulation:
I. Pre-glomerular vasoconstriction – sepsis, NSAIDs
II. Post-glomerular vasodilatation – ACEi, ARBs
Acute tubular necrosis is volume unresponsive AKI.
Identify three of its causes
- Ischaemia (depletion of cellular ATP)
- Nephrotoxins
- Sepsis
Describe the pathophysiology of ATN
⇒ Death of tubular epithelial cells
⇒ Damaged cells cannot reabsorb / expel excessive H2O efficiently
⇒ Aggressive fluid resuscitation risks fluid overload
Describe the course of renal blood flow
Identify the sites of tubular injury in ATN
Compare and contrast the urinary biochemistry of Pre-renal AKI and ATN in terms of:
- Specific gravity
- Osmolality
- Urinary Na+
Nephrotoxins can be endogenous or exogenous.
Identify some examples of each
What is myoglobinuria and how does it present?
Myoglobinuria is the presence of myoglobin in the urine usually associated with rhabdomyolysis or muscle destruction
In 5 steps, explain how thrombotic microangiopathy leads to microangiopathic haemolytic anaemia
⇒ Endothelial damage
⇒ Platelet thrombi
⇒ Partial obstruction of small arteries
⇒ Destruction of RBC’s
⇒ Microangiopathic haemolytic anaemia occurs
Describe the pathophysiology of post-renal AKI
⇒ Obstruction with continuous urine production
⇒ Rise in intraluminal pressure
⇒ Dilatation of renal pelvis (hydronephrosis)
⇒ Decrease in renal function
