Flashcards in Week 9 - Acute Kidney injury Deck (55):
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?
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?
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?
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?
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?
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?
-drugs eg gentamycin, NSAIDs
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
What is wegners granulomatosis?
-Rapid progressive glomerulonephritis with granulomatosis and polyangitis
Name a primary glomeruonephritis
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
-Cannot lie still
What U+E results would indicate AKI?
-Hypocalcaemia and hyperphosphataemia
What ECG changes signify hyperkalaemia?
-Tall, tented T waves
-Small/absent P waves
-Increased PR interval
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
-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
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
Describe some risk factors for developing AKI
How do you manage patients in volume overload?
-Restrict dietary Na and water intake
How do you manage hyperkalaemia?
-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
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