Ch. 30 Renal - Book/2 Flashcards
intrarenal/intrinsic AKI can result from
ischemic acute tubular necrosis ATN
prerenal AKI - poor perfusion can result from
5
- hypotension
- hypovolemia associated with hemorrhage or fluid loss i.e. burns
- sepsis
- inadequate CO i.e. MI
- renal vasoconstriction i.e. NSAIDs
what provide an index of renal function during the AKI recovery phase
plasma creatinine concentrations
AKI - prevention of injury is possible in which phase
initiation
renal failure refers to
significant loss of renal function
prevention of AKI involves avoidance of
3
- hypotension
- hypovolemia
- nephrotoxicity
postrenal AKI usually occurs with
UTO that affects the kidneys bilaterally
when less than 10% of renal function remains, this is termed
ESKD
AKI type - renal vasoconstriction i.e. NSAIDs
pre
anuria suggests
bilateral renal artery occlusion
caused by inadequate kidney perfusion
prerenal AKI
increased blood urea nitrogen levels and frequently increased serum creatinine levels
azotemia
rare AKI
post
what can serve as a measure of GFR (serum protein)
cystatin C
sudden decline in kidney function with a decrease in glomerular filtration and urine output with accumulation of nitrogenous waste products in the blood
AKI
interval when glomerular function returns but the regerating tubules cannot concentrate the filtrate
AKI recovery/polyuric phase
postrenal AKI causes an increase in intraluminal pressure upstream from the site of obstruction with gradual what
decrease in GFR
AKI maintenance phase is the period of
established kidney injury and dysfunction after initiating event has been resolved
renal insuff levels of serum creatinine and urea are
mildly elevated
AKI results from
4
- ischemic injury related to extracellular volume depletion
- ischemia from decreased renal blood flow
- toxic injury from chemicals
- sepsis-induced injury
AKI maintenance phase aka
oliguric phase
AKI phase in which reduced perfusion or toxicity in which kidney injury is evolving
initiation
anuria is uncommon in
ATN