Acute Kidney Injurty Flashcards
What are the definitions of AKI?
Increase in serum creatinine over a period of itme
reduction in urine output over a period of time
How do we classify AKI?
By the likelihood of kidney damage depending on how far the creatinine / urine output changed
What are the common causes of AKI?
acute tubular necrosis (damaged infrastructure)
pre-renal (hypoperfusion to kidney) by burn, sepsis, dehydration, haemorrhage
acute onset chronic renal failure
obstruction (both kidneys need to be blocked)
acute interstitial nephritis (hypersensitivity reaction) - reaction to PPI, drugs
RPGN, vascular
Why is kidney susceptible to nephrotoxicity?
because of high blood supply and toxin concentrations in renal cells
What can reverse the injury during initiation?
restoration or reperfusion
How long is the maintenance stage and what can be seen?
7-14 days, GFR is depressed and metabolic consequences can be seen
What happens during the recovery stage?
tubule cell regeneration, gradual return of GFR over 2-3 weeks
What are the common causes of death nowadays?
sepsis, CDV, pulmonary dysfunction, withdrawal of life-support
Triple whammy includes….
ACEI/ARB + NSAIDS + diuretics
What do NSAIDs do in triple whammy?
block PGI2/ PGE2
How is low BP usually fixed in normal condition?
extra renally: by vasoconstriction
renally: increased PGI2/PGE2 which decreases renal blood flow, GFR, and increase sodium and water retention
What is one good and bad point about ACEI/ARB in terms of AKI?
It prevents progression to in stage chronic renal failure BUT
it can CAUSE acute renal failure
When should we withdraw ACEI to avoid nephrotoxicity?
If Cr increases more than 25% above baseline which the first 2 months of therapy
What can increase the level of Cr?
Increase in COPD drug dose, and rhabdomyolysis by statins
What can you see in the lab test of someone with rhabdomyolysis?
VERY high CK, hyperkalaemia, hyperuricaemia, hyperphophataemia, HYPOcalcaemia
