Acute Renal Failure CIS Flashcards
aleve
NSAID
elevated creatinine
represent renal failure**
creatinine represents
GFR
acute kidney injury
acute renal failure
- 50% increased in serum Cr
- increase in serum Cr - 0.3
- reduction in urine output less than 0.5 longer than 6 hours
acute or chronic kidney problem?
- sediment
- kidney size
- compare previous Cr
acute sediment
active - casts
chronic sediment
bland
acute kidney size
normal
chronic kidney size
small and scarred
stigmata for chronic renal failure
- anemia
- hyperPTH
- A/V fistula
- hyperP
acute kidney injury
prerenal
renal
post renal
renal causes of acute kidney
ischemia toxic glomerulonephritis acute interstitial nephritis renovascular obstruction
endogenous toxins
cause AKI > renal > toxic
-Mg, Hg, light chain, calcium, uric acid
hyaline casts
prerenal AKI**
muddy brown casts
intrarenal tubular cell injury
-ATN** - acute tubular necrosis
epithelial casts
eosinophils
intrarenal - interstitial nephritis
RBC casts
glomerularnephritis AKI
FeNa
urine Na x plasma Cr x 100 / plasma Na x Urine Cr
pre-renal FeNa
<10
urine Na
usually looked a for AKI work up
low in pre-renal
high in renal - can’t reabsorb
prerenal urine Na
<10
ATN urine Na
> 20
toxic injury urine Na
> 20
renal ultrasound
hydronephrosis kidney size cysts stones tumors
prerenal azotemia
no change to kidney
-hypoperfusion will recover normally
causes of prerenal azotemia
shock , dehydration, hemorrhage, sepsis, vomiting, diarrhea, sweating, diuretics, DM, cirrhosis, CHF, hepatorenal syndrome, peritonitis, hepatorenal syndrome, renal a stenosis, embolism
meds make prerenal azotemia worse
NSAIDs ACE (-) diuretics contrast dye tacrolimus cyclosporine ARBs
urinary sodium >20
think acute tubular necrosis
acute interstitial nephritis
with NSAIDs
upper GI bleed
can result in very high BUN
muddy brown casts
ATN
-acute tubular necrosis
stages of ATN
initiation - polarized cell
extension - depolarized cell
maintenance - dedifferentiated cell
recovery - polarized again
usually takes 1 week to recover**
initation of ATN
falling GFR
polarized cell
extension of ATN
depolarized cell
- apoptosic/necrosis/lumen obstruction
- GFR falling
maintenance of ATN
dedifferentiated cells are reestablishing as tubular epithelium
recovery of ATN
cell repolarization
-GRF rising
neurogenic bladder
can be due to multiple sclerosis
-Tx catheter
unilateral ureter obstruction
causes postrenal azotemia if they have one kidney or chronic kidney disease
majority of postrenal azotemia
from bilateral ureter obstruction
nephrotoxic meds
aminoglycosides contrast acyclovir cisplatin sulfa methotrexate cyclosporine tacrolimus amphotericin B foscarnet pentamidine ethylene glycol toluene cocaine HMG-CoA recuctase (-)
legs petechia, lung consolidations, RBC casts in urine,
wegeners granulomatosis
causes of acute interstitial nephritis
beta-lactam antibiotics
diuretics
other antibiotics
NSAIDs
**eosiniphils in urine, rash, and elevated Cr
RBC casts
something wrong with glomerulus
wegeners
kidney, lung, sinus
goodpasture
anti-GBM antibodies
wegeners
c-ANCAs
polyareritis nodosa
p-ANCAs
final step if nothing else works
urinalysis, ultrasound, antibody check
do biopsy
