Acute kidney injury Flashcards
Dr. Covert EXAM 2
AKI Staging: Urinary output
Normal: 0.5ml/kg/h
Non-Oliguric: > 500ml/day
Oliguric: < 500ml/day
Anuric (no urine): <50 ml/day
AKI Staging: SCr
AKI if:
increase in SCr by >0.3 mg/dl within 48h
increase in SCr by 1.5x baseline occurred within 7 days
-UOP < 0.5 ml/kg/hr (less than optimal urine output) for 6 hours
What is used to define the severity of AKI after AKI is diagnosed?
-RIFLE (change in renal function within 7 days)
-AKIN ((change in renal function within 48 hours)
(could be on the NAPLEX)
RIFLE and AKIN
RIFLE
as the stage gets severe,
SCr: goes up (worse)
UOP: decreases
GFR: decreases
AKIN
SCr: goes up (worse
UOP: decreases
Types of AKI
-Prerenal (70%)
-Intrinsic/Functional
-Postrenal/Obstructive
Pathophysiology of Prerenal AKI
the kidneys are not being perfused appropriately (not enough blood perfusion)
-Volume depletion: insufficient water intake, diarrhea/vomiting, diarrhetic use, blood loss (decreased circulation)
-decreased circulation: low BP, blood loss,
-Functional: drug-related poor perfusion, ACEi, ARBs, NSAIDs
Diagnosing prerenal AKI
-Urinalysis: specific gravity (concentrated urine) and urine sediments -> Hyaline casts
-Fe(Na): fractional excretion of sodium - impacted by diuretics - preventing Na from bein reabsorbed (higher amount in the urine) !! -> use Fe(urea) for patients who are on diuretics
Fe(Urea): fractional excretion
What impacts the FeNa equation?
Diuretics
-use Fe(Urea)
Fe(Na)
MEMORIZE
[U(Na)*SCr] / [U(Cr) * S(Na)] * 100
<1%, prerenal AKI
>2% potentially intrinsic AKI
What Fe(Na) is expected in a patient who is not hydrated?
low Fe(Na), because the body try to prevent escaping of Na into the urine
Q: Prevention of Na filtration??? and how???
is the filtration of Na passive???
Treatment of Prerenal AKI
Volume Depletion: fluid resuscitate (IV or oral fluid depending on the severity)
Decreased Circulation:
treat the cause: Hypotension due to heart failure or cirrhosis; Hypotension due to Sepsis, drug-induced hypotension (f.e. increased the dose of lisinopril to 40mg -> caused hypotension -> lower the dose back to 20mg
Functional: remove the offending agent if possible (if they really need ACEi or ARB make a risk/benefit assessment)
Intrinsic AKI
Direct renal damage -> based on where the damage is: Tubular, Glomerular, Interstitial, Vascular
Tubular AKI
Acute Tubular Necrosis (ATN) 85% of intrinsic AKI
can be ischemic: prolonged hypotension
can be drug-induced
-often fluid doesn’t help -> dialysis
Glomerular AKI
Glomerulonephritis (often a complication of another disease)
-f.e. lupus nephritis
-Nephritic vs Nephrotic
-treat primary disease
ATN vs AIN
ATN: direct damage to the kidney
AIN: allergic (immune) response