Week 9 - Acute Kidney injury Flashcards
How is GFR measured?
-Measure in serum creatinine
Why is AKI treated as a medical emergency?
-Delayed treatment leads to irreversible renal failure
What are the three groups of causes of AKI?
- Pre-renal
- Intrinsic renal
- Post-renal
What type of injury cause pre-renal failure?
-Anything which causes volume depletion to the kidney eg heart failure, cirrhosis
What type of diseases cause intrinsic renal AKI?
-Any kind of necrosis or ischaemia which affects the parenchyma eg glomerulonephritis, Acute Tubular Necrosis
What type of injury causes post-renal AKI?
-Anything which obstructs the urinary tract eg stones, prostate hyperplasia
What is the major cause of AKI?
-Acute tubular necrosis
Describe the pathophysiology of pre-renal AKI
- Reduced renal blood flow reduces GFR
- There is no cellular damage so kidneys work hard to restors bloodflow and avidly resorb salt and water
Does pre-renal AKI respond to fluid resuscitation?
Yes
Describe urine production in pre-renal AKI
-Little and concentrated because reabsorbing fluid
Why is hypertension significant in pre-renal AKI?
-Blood pressure may seem adequate however the patient may normally have high BP so their current BP is low and the person is at risk of pre-renal AKI
Describe autoregulation in pre-renal AKI
- Reduced renal perfusion causes vasodilation of afferent arteriole to increase renal blood flow
- Vasoconstriction of efferent arteriole to increase renal blood pressure
- Attempts to maintain GFR
Why does AKI occur in pre-renal states?
-Autoregulation becomes overwhelmed and cannot maintain GFR
At what pressures is autoregulation able to work?
-80-180mmHg
Name 2 drugs which can override autoregulation and explain why?
- NSAIDs -> inhibit prostaglandin production -> inadequate vasodilation of afferent arteriole
- ACE inhibitor -> inhibits angiotensin II which acts as a vasoconstrictor of efferent arteriole
What develops from pre-renal AKI if the underlying cause is not treated?
-Acute tubular necrosis
What are the major causes of acute tubular necrosis?
- Ischaemia
- Necrosis
- Sepsis
What is acute tubular necrosis?
-Injury to proximal tubular cells which results in inability to resorb salts and water efficiently or expel excess water
Does ATN respond to fluid resuscitation?
-Sometimes but high risk of fluid overload
Is AKI reversible?
-Potentially yes
When does mortality significantly increase in AKI?
-If dialysis is required
Describe the pathophysiology of ischaemic necrosis
- The PCT is the most susceptible area to hypoxia as it has the higest O2 demand
- Any cause of hypoxia to the cells results in injury and the cells can no longer function
Describe the urine produced in ATN
-Often copious and dilute
Describe the pathophysiology of toxin ATN
- Nephrotoxins damage epithelial cells lining tubules and cause shedding into lumen
- ATN is much more likely to occur if there is reduced perfusion and presence of a nephrotoxin
Name some endogenous nephrotoxins
-Myoglobin, bilirubin, urate
NAme some exogenous nephrotoxins?
- Endotoxin
- X-ray contrast
- drugs eg gentamycin, NSAIDs
- Poisons
What is rhabdomyolysis and why can it cause AKI?
- Muscle necrosis, often due to crush injuries, causes release of myoglobin
- Myoglobin is filtered at the glomerulus and is toxic to tubule and may cause obstruction -> causes AKI
What is characteristic of rhabdomyolysis?
-Produces black urine
What is acute glomerulonephritis?
- Immune diseases which affect the kidney
- Can by primary and only affect the kidneys or secondary as part of a systemic process
Name some secondary glomerulonephritis
- Systemic lupus erythema
- Vasculitis
What is wegners granulomatosis?
-Rapid progressive glomerulonephritis with granulomatosis and polyangitis
Name a primary glomeruonephritis
-IgA nephropathy
Name 2 causes of acute tubulo-interstitial nephritis
- Infection eg acute pyelonephritis
- Toxin-induced eg NSAIDs
Describe the pathophysiology of post-renal AKI
- Obstruction which blocks both kidneys causes an increase in intraluminal pressure as urine is continually being produced
- This causes dilation of renal pelvis (hydronephrosis)
- Decreased renal function
What 3 groups can cause obstruction AKI?
- Within the lumen eg stones, tumours
- Within the wall, stricture post TB, congenital megaureter
- Pressure from outside eg enlarged prostate, tumour, aortic aneurysm
What criteria must stones meet to cause AKI?
-Must be in neck of bladder, urethra or both ureters
What are the common signs of renal stones?
- Loin to groin pain
- Haematuria
- Cannot lie still
What U+E results would indicate AKI?
- Hyponatraemia
- Hyperkalaemia
- High urea
- High creatinine
- Hypocalcaemia and hyperphosphataemia
What ECG changes signify hyperkalaemia?
- Tall, tented T waves
- Small/absent P waves
- Increased PR interval
- Widened QRS
Describe signs which would point towards the patient being volume depleted
-Cool peripheries, increased pulse, low bp, dry axillae
Describe signs which would point towards the patient being fluid overloaded
-Gallop rhythm, pulmonary oedema, peripheral oedema
What is mandatory in every patient with AKI?
-Urinalysis using dipstick for blood, protein and leukocytes
Describe how AKI is investigated
- Urine dipstick, culture and chemitry
- USS, CXR
- Biopsy if appropriate
When do you use USS in AKI?
-Post-renal or pre-renal/ATN not improving
When do you biopsy in AKI?
- Pre and Post-renal ruled out
- Confident ATN diagnosis cannot be made
- SIRS present
What is the main priority in AKI?
-BP and blood vol followed by pH and hyperkalaemia then watse and drug metabolism
How do you prevent AKI?
- Identify risk factors and monitor at-risk patients
- Ensure adequate hydration
- Avoid nephrotoxins
Describe some risk factors for developing AKI
- Advanced age
- CKD
- Heart/liver disease
- Sepsis/critical illness
- Burns/trauma
How do you manage patients in volume overload?
-Restrict dietary Na and water intake
How do you manage hyperkalaemia?
- Calcium gluconate
- IV insulin + dextrose
- Restrict dietary K
- Stop K sparing diuretics and ACEI
What are indications of AKI for dialysis?
- High K+ non-responsive to treatment
- Fluid overload despite diuretics
- Metabolic acidosis where NaHCO3 not appropriate
- Presence of dialysable nephrooxin
- Signs of uraemia
Describe some signs of uraemia
- Pericarditis
- Reduced consciousness
- Intactable N&V
Describe the prognosis of uncomplicated ATN
- Expect recovery in 2-3 weeks
- Mortality varies from 30-80%
Patients who experience AKI are at risk of what in later life?
- Higher risk of death for 1 year
- Higher risk of developing CKD
What is acute kidney injury?
-Clinical syndrome characterised by an abrupt decline in GFR, upset of ECF volume, electrolyte and acid-base homeostasis and accumulation of nitrogen waste products
