Aki Flashcards
What is aki
- Clinical syndrome
- Abrupt decline in actual GFR (days to weeks)
- Upset of ECF volume, electrolyte and acid-base homeostasis • Accumulation of nitrogenous waste products
What defines aki
• AKI defined by any of the following:
• 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
What are the causes of aki
• Pre-renal failure • Intrinsic renal failure - artery occlusion, vasculitis - small vessel disease - glomerular disease - acute tubular necrosis - acute interstitial nephritis - intertubular obstructoin • Post-renal failure (obstruction)
Describe pre renal aki
- Actual GFR reduced due to decreased renal blood flow
- No cell damage so kidneys works hard to restore blood flow
- Avidly reabsorption of salt and water (aldosterone and ADH release)
- Responds to fluid resuscitation i.e. potentially reversible
Describe renal autoregulation
Ss
Can lose a lot of blood pressure before cerebral blood flow drops . Get a drop in perfusion eventually it will fall.
But in chronic hypertension - evidence in dehydration by change in kidney function
Rewatch
What is a physiological mechanism to decrease in pressure
- vasoconstriction the efferent arteriole. Increase pressure.
Afferent - dilation. More blood getting to kidney, more difficult to elave
Increase pressure
• In mild hypoperfusion, autoregulation ensures renal
blood flow preserved. • If compensatory responses are overwhelmed, AKI
occurs. • Autoregulation causes maximal dilatation of arterioles
at systolic BP 80mmHg (higher if hypertensive), below
this GFR falls rapidly
How to acei and nsaids affect renal perfusion
Can override intrinsic autoregulatory mechanisms
NSAIDs stop PGs vasodilation anf acei stop angii vasoconstriction
Disease of the afferent arteriole (BP, progressive kidney disease, DM) can result in too great or too little a response to these stimuli
More at risk of aki bc not as able to auto regulateaaaa
What are causes of pre renal aki
Ss
Can pre renal aki be corrected?
Pure pre renal renal failure - can be reversed if you dont get too acidosis - have a window where can be improved to stop cell necrosis. . If you miss the therapeutic window - cellular damage occurs - atn. Cells die. . Eg f they dont get to hospital or dont get antibiotics in time
What is atn
‘ATN’ – ‘Acute tubular necrosis’
• Can be caused by
– Ischaemia (depletion of cellular ATP)
– Nephrotoxins
– Sepsis
• Often a combination of 2 or more
• A misnomer
• A misnomer as generally not tubular necrosis but cells damaged therefore cannot be immediately reversed
• Damaged cells cannot reabsorb salt and water efficiently or expel excess water
Aggressive fluid resuscitation risks fluid overload
Compare prerenal vs atn
Ss
How can nephrotoxis affec the kidney
• Nephrotoxins damage the epithelial cells lining the tubules and cause cell death
• Nephrotoxins can be endogenous or exogenous
• ATN is much more likely if there is reduced perfusion and a
nephrotoxin
• In a patient with AKI, consider whether any of the drugs the patient takes could be contributing
What are some endogenous and exogenous nephrotoxins
Endo -
Myoglobin
Irate
Bilirubin
Exo- X-ray contrast Endotoxins Drugs eg NSAIDs, gentamicin Poison eg antifreeze
What is rhabdomyolysis
• Due to muscle necrosis - release of myoglobin
• ‘Crush injury’
• AKI in wars / natural disasters (earthquakes)
• Drug users (unconscious so don’t move)
• Elderly – fall and unable to get up
• Myoglobin filtered at glomerulus and toxic to tubule cells. Can
also cause obstruction
People falling over, crush injury to muscle, muscle broken down, myoglobin filtered by kidney, loss of kidney function, need dialysis,
Coca Cola urine
Ck high
What are other intrinsic causes of aki
Ss
