Renal Approach To AKI and Renal Failure - Dr. Grin Flashcards
AKI is seen from what
elevated Cr
= which can cause high urea, electrolyte imbalance and volume overload
AKI Dx how
- increase in serum Cr by > 0.3mg/dL in 48hrs
- increase serum Cr > 1.5 times higher then BASELINE
- Decrease urine volume
reason AKI you need to compare Cr to baseline
more muscular pts have higher Cr levels
Cr and eGFR relationship in AKI
inverse
as Cr goes us, eGFR goes down (esp early increase)
Anuria Oliguria Azotemia Pre-renal Azotemia Uremia
Anuria = less then 100ml/day
Oliguria = under 400-500ml
Azotemia = high BUN
Pre-renal Azotemia = high BUN not proportional to Cr
Uremia = high BUN + sx like confusion, n, v, metallic taste
AKI sx you usually see
aymptomatic = htn = edema = dyspnea = uremia
uremia sx you can see in physical exam
- Asterixis (also seen in cirrhosis)
2. uremic frost (white crystal on feet)
AKI prerenal
- hypovolemia (bleeding, V,D)
- Hypervolemia (CHF)
- drugs impairing renal regulations (NSAIDs, ACEI)
- sepsis, SIRS, cirrhosis = vasodilation
AKI intrinsic renal
- acute tubular necrosis (can happen from prerenal, uric acid, myeloma LCs, IV contrast, mygobulin)
- Acute interstitial nephritis (PPIs, NSAIDs, ABs some)
- Glomerular disease (post strep GN)
- vascular (vasculitis, malignant htn, TTP/HUS)
AKI postrenal
- Bladder outlet obstruction (BPH, Blood clot)
2. Ureteral obstruction : stone, compressed from malignancy
AKI prerenal tx
reverse BF (most common cause is dehydration
labs that show AKI from prerenal cause**
- urine NA < 20mEg/L
- BUN/Cr > 20:1
- Urine osmolality > 500mosm/kg
prerenal meds
NSAIDS : X vasodilation afferent (coming)
ACEI : X constrict efferent arteriole (leaving)
Acute Tubular necrosis
renal tubular cells die and slough off and clog tubules = decrease GFR
- sepsis
- myoglomin =rhbdo
- LCs
- IV contrast
prerenal vs ATN
prerenal is reversible before interstitial AKI ATN