Acute Kidney Injury (Exam 2) Flashcards
acute kidney injury (aki)
abrupt decline in renal function
inability to properly excrete waste and maintain acid base balance
clinical definitions of AKI (4)
decrease of 25% or greater in estimated GFR
an increase in SCr of 0.5mg/dL or greater
an increase of 1mg/dL or more in SCr in pts with CKD
urine output <0.5mL/kg/hour for at least 6 hours
anuria urine output
<50 mL/day
non-oliguria urine output
greater than 500mL/day
better outcome
oliguria urine output
> 50mL but less than 500mL/day
normal urine output
1mL/kg/hour
diagnostic criteria for acute kidney injury network
an absolute increase in SCr of more than 0.3mg/dL
an increase in baseline SCr by 50% or more
urine output of less than 0.5mL/kg/hour for more than 6 hours
AGENTS used to treat/prevent AKI
thiazide diuretics
loop diuretics
potassium-sparing diuretics
thiazide diuretics
chlorothiazide - diuril
chlorthalidone
hydrochlorothiazide - microzide
indapamide
metolazone
loop diuretics drugs
bumetanide - bumex
ethacrynic acid - edecrin
furosemide - lasix
torsemide - demadex
potassium-sparing diuretics
amiloride
eplerenone - inspra
spironolactone - aldactone, carospir
triamterene - dyrenium
loop diuretics increase
renal blood flow and urine flow
General principles for prevention of AKI (4)
avoid nephrotoxic agents
ensure adequate hydration
patient education
drug therapies to decrease incidence of contrast induced nephropathy
N-acetylcysteine (NAC)
contrast induced nephropathy
well tolerated, little adverse effects
goals of therapy for AKI (5)
maintain appropriate BP
monitor and manage electrolytes daily
eliminate or minimize insult that precipitated AKI
facilitate renal recovery and minimize injury
expedite recovery of baseline renal function
Mannitol MOA
increases the osmotic pressure of glomerular filtrate which inhibts tubular reabsorption of water and electrolytes
what does Mannitol induce?
hyperosmolar state
loop diuretics have no benefit for ____ and are _____. Switching loop diuretics is _______.
survival outcomes
equally effective
unlikely to be effective
proximal tubule (PCT) components
NaHCO3
Na+
Cl-
H2O
Glucose
Amino Acids
thick ascending limb of loop of henle (TAL) components
Na+
K+
Cl-
Mg2+
Ca2+
Distal convoluted tubule (DCT) components
Na+
Cl-
Ca2+ (PTH)
Thin descending limb of loop of Henle components
H2O
what is diuretic resistance?
not responding to loop diuretics
Collecting duct components
Na+
Cl-
K+ (secretion)
H+ (secretion)
ACEIs
angiotensin-converting enzyme inhibitors
NSAIDs
nonsteroidal anti inflammatory drugs
A (indications for RRT)
acid base abnormalities
E (indications for RRT)
electrolyte imbalance
I (indications for RRT)
intoxications
O (indications for RRT)
fluid overload
U (indications for RRT)
uremia
DIKD (drug induced kidney disease) primary prevention strategy
avoid use of nephrotoxic agents
AKI characteristics
fluid overload
acid base abnormalities
increased serum Cr and BUN
AKI can further classify into stages 1-3 on the basis
of degree of SCr rise and urine output
RIFLE category
risk
injury
failure
loss
ESKD
risk urine output criteria
less than 0.5 mg/kg/h for 6 hrs
injury urine output criteria
less than 0.5 mg/kg/h for 12 hrs
failure urine output criteria
anuria for more than 12 hrs
AKIN criteria
Stages 1-3
AKIN stage 1 urine output criteria
less than 0.5 mg/kg/h for 6 hrs
AKIN stage 2 urine output criteria
less than 0.5 mg/kg/h for 12 hrs
AKIN stage 3 urine output criteria
less than 0.3 mg/kg/h for 24 hours OR anuria form more than 12 hrs
KDIGO criteria
stages 1-3
KDIGO stage 1 urine output criteria
less than 0.5 mg/kg/h for 6 hrs
KDIGO stage 2 urine output criteria
less than 0.5 mg/kg/h for 6-12 hrs
KDIGO stage 3 urine output criteria
anuria for more than 12 hrs
RIFLE category is based off of ?
AKIN and KDIGO criteria are based off of ?
RIFLE - SCr and GFR
AKIN/KDIGO - SCr
loop diuretics are useful for
management of fluid overload for patients at risk for AKI
DOES NOT prevent
nonpharmacologic therapy for AKI
avoid nephrotoxic agents
hydration
RRT - dialysis
Target for UOP - greater than 0.5 mg/kg/h
pharmacologic therapy for AKI
diuretics
mannitol
why does someone on Mannitol have to be closely monitored?
it can cause AKI
dose of Mannitol
12.5-25 grams IV over 3-5 minutes
parenterally
most common loop diuretic used
furosemide
torsemide and bumetanide have
greater oral bioavailability and are more potent
which type of drugs are recommended for prevention in AKI?
Isotonic Saline IV
vasopressors
which type of drugs are recommended for prevention in contrast induced AKI?
isotonic saline IV
NAC (n-acetylcysteine)
Sodium bicarbonate IV
monitoring parameters for AKI
fluid ins/outs
weight
hemodynamics
blood chemistries
drugs, dose regimens and times of doses
nutritional regimen
blood glucose
urinalysis
plans for RRT
Acute Tubular Necrosis
damage to tubule cells of the kidneys
proximal and distal tubules
the most common cause of AKI
acute tubular necrosis
ATN can be caused by
aminoglycosides
radiocontrast media
amphotericin B
Osmosis nephrosis
swelling of the renal proximal tubular cells associated with glomerular filtration of sugars and dextrose
contrast media induced nephrotoxicity
any combination of direct tubular toxicity, renal ischemia and tubular obstruction
examples of CM induced nephrotoxicity drugs
ethiodol
lipiodol
diatrizoate
iothalamate
gadodiamide
gadobutrol
perflutren
CM induced nephrotoxicity incidence
7-15% - receiving iodinated contrast
2% - normal renal function
over 50% - CKD
Biomarkers of AKI
cystatin C
IL -18
KIM-1
NGAL
cystatin c source
plasma and urine
IL-18 source
urine
KIM-1 source
urine
NGAL source
plasma and urine
which is the most sensitive biomarker for AKI?
NGAL (neutrophil gelatinase associated lipocalin)
how much of the three criteria of AKI is required and in what time frame to give a diagnosis (according to the diagnostic criteria)?
one of the three criteria within 48 hours