AKI Flashcards
Define AKI
Increase in serum creatinine by >26.5 umol/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 is the difference between stage 1-3 of AKI?
1 - Cr> 150-200% from baseline, <0.5ml/kg/hr for >6hours
2 - Cr > 200-300%, <0.5ml/kg/hr for >12hours
3 - Cr > 300% from baseline or initiated on RRT, <0.3ml/kg/hr or anuria for 12hours
Why is AKI important?
It is a powerful marker for mortality - 1/3 of people with stage 2/3 AKI will die.
What is the incidence of AKI?
10% of hospitalised patients will develop AKI.
25-30% of patients in ITU.
What are the causes of AKI?
1 - pre-renal renal failure - not enough blood, most common
2 - Renal
3 - Post-renal - Bladder obstruction, tumour, renal calculi, papillary necrosis, retroperitoneal fibrosis.
Why does pre-renal AKI occur?
Actual GFR reduced due to decreased renal blood flow.
No cell damage so kidney works hard to restore blood flow.
Avidly reabsorption of salt and water (aldosterone and ADH released)
Responds to fluid resuscitation (reversible)
What is the role of auto regulation?
Autoregulation is when the kidney controls its own blood flow to maintain GFR despite the change in blood pressure.
If compensatory responses are overwhelmed, AKI occurs.
Autoregulation causes maximal dilatation of arterioles at systolic BP 80mmHg (higher if hypertensive), blow this GFR rapidly.
How do ACE inhibitors and NSAIDs affect renal perfusion?
Can override intrinsic auto-regulatory mechanisms.
NSAIDs - prevent vasodilation of afferent arteriole by prostaglandins.
ACE-I - Prevent vasoconstriction of efferent arteriole by angiotensin II.
What could cause prerenal AKI
Reduce effective arterial blood volume:
- Hypovolaemia (blood / fluid loss)
- Systemic vasodilation(sepsis, cirrhosis, anaphylaxis)
- Cardiac failure
Impaired renal autoregulation:
- Pre-glomerular vasoconstriction (sepsis, drugs)
- Post-glomerular vasodilation (Acei, AIIR antagonists)
What could cause ATN?
Acute tubular necrosis:
- Ischaemia
- Nephrotoxins
- Sepsis
Often a combination fo 2 or more.
Define ATN
Misleading as generally not tubular necrosis. But cells damaged therefore cannot be immediately reversed.
Damage cells cannot reabsorbed salt / water efficiently or expel excess water.
What is the difference between pre-renal and ATN?
Pre-renal has a higher specific gravity (>1.018 whereas ATN >1.012)
Pre-renal has a high osmolality (>500mosm/kg whereas ATN <250mosmol/kg)
ATM has at least double the amount of Na in the urine (>20mmol/L whereas Pre-renal <10mmol/L)
What are nephrotoxins?
Nephrotoxins damage the epithelial cells lining the tubules and cause cell death.
They can be endogenous (myoglobin, urate, bilirubin) or exogenous (endotoxins, X-Ray contrast, Drugs, poisons)
What is rhabdomyolysis?
Muscle necrosis due to release fo myoglobin.
‘Crush injury’
AKI in wars / natural disasters (earthquakes)
Drug users (don’t move)
Elderly - fall and unable to get up
Myoglobin filtered at glomerulus and toxic to tubule cells. Can also cause obstruction.
Treat with IV fluids.
What is vasculitis?
Vasculitis is a group of disorders that destroy blood vessels by inflammation.
Primarily caused by leukocyte migration.
