AKI-Clinic VIR Flashcards
(35 cards)
definition of kidney injury/disease
alteration in kidney structure or function such than GFR is less than 60
chronic kidney disease must last greater than or equal to?
3 months
limitations to serum creatinine as measure of kidney function
does not truly reflect decrease in GFR until 3 days after insult begins; affected by body mass, hydration, etc.
signs of acute vs. chronic kidney disease
acute: decreased urine output; chronic: small, echogenic kidneys on US
most common cause of AKI in community is ____, in hospital is _____
pre-renal (ischemia or nephrogenic); intra-renal (especially tubular injury)
causes of decreased renal perfusion (pre-renal ischemia)
low ECF volume (GI loss, hemorrhage, diuretics); altered blood flow (sepsis, heart failure, cirrhosis, hypercalcemia, medications, vascular dz)
causes of acute tubular necrosis (intra-renal)
ischemic tubular injury (from pre-renal cause oftentimes) or nephrotoxins (cisplatin, aminoglycosides, heme, iodinated radiocontrast)
causes of post-renal injury
prostate hypertrophy, kidney stones
diagnostic approach to evaluating AKI
- history, 2. physical exam, 3. exclude urinary tract obstruction, 4. examine urine
what component of the physical exam is particularly important when dx AKI
volume status: are there signs of volume depletion (skin turgor, orthostatic hypoTN)? If so, then likely PRE-RENAL
how do you exclude post-renal causes of AKI?
insert foley catheter and observe no change in urine output; renal US demonstrates cortex of normal thickness, no dilation in collecting system
urine sediment will look ____ if pre-renal injury
normal
causes of RBC casts and proteinuria in the urine
glomerulonephritis, vasculitis, TMA, atheroemboli
causes of WBC casts and eosinophils in urine
pyelonephritis, interstitial nephritis, atheroemboli, glomerulonephritis
cause of renal tubular endothelial cells and dark muddy casts in urine
ATN
the most important distinction to make when analyzing urine indices is between ____ and ____
pre-renal and ATN
describe the SG, osmolality, sodium, FENa, and FEUrea for pre-renal tubular injury
SG >1.020, osmol >500, Na <35% (so basically higher SG and osmolality, lower excretion of sodium and urea)
describe the SG, osmolality, sodium, FENa, and FEUrea for ATN
SG ~1.010, osmol 30, FENa >2%, FEUrea >50% (so basically lower SG and osmolality, higher excretion of sodium and urea)
why is FE (fractional excretion) used to measure sodium and urea excretion?
unaffected by water reabsorption
how to calculate FENa
Na excreted/Na filtered X 100 = (UNa X SCr)/(UCr X SNa) X 100
when should FE Urea be used instead of FE Na?
when diuretics have been given in past 24-48 hours (b/c urea is reabsorbed before you get to action of diuretics)
when might FE Na be greater than 2% in a setting other than ATN?
CKD, recent diuretic use
when might ATN present with an FE Na of <1%?
if it is from radiocontrast, is early (nonoliguric), or is co-occuring with chronic pre-renal condition
what is an example of an intra-renal process that causes an FE Na of <1%?
glomerulonephritis/vasculitis
