Acute Kidney Injury (AKI) Flashcards
(31 cards)
Define: Acute Kidney Injury
acute worsening in renal function
Define: Oliguria
urine output (UOP) < 500 mL/day
Define: Anuria
urine output (UOP) < 50 mL/day
What are the risk factors of AKI?
-sepsis/critical illness
-dehydration
-burns
-trauma
-surgery
-nephrotoxic drugs
-contrast agents
-advanced age
-female gender
-CKD
-diabetes
-cancer
KDIGO AKI DEFINITION
increase in serum creatine (SCr) by 0.3 mg/dL within 48h OR increase in SCr to > 1.5 times baseline occurring within prior 7 days OR urine volume <0.5 mL/kg/h for 6+ hours
RIFLE CRITERIA
-RISK= SCr increase 1.5-1.9x baseline or decrease in GFR >25% OR UOP 0.5mL/kg/h in 6 h
-INJURY= SCr increased 2-2.9x baseline or decrease in GFR >50% OR UOP <0.5mL/kg/h for 12 h
-FAILURE= SCr >3x baseline, decrease in GFR >75%, or 4 mg/dL OR UOP <0.3 mL/kg/h for 12 h or anuria for >12 h
-LOSS= persistent renal failure > 4 weeks
-END-STAGE RENAL DISEASE= persistent renal failure > 3 months
Define: AKIN Stage 1
SCr increase 0.3 mg/dL or 1.5-2x baseline OR UOP <0.5mL/kg/h in 6h
Define: AKIN Stage 2
SCr increase 2-3x baseline OR UOP <0.5 mL/kg/h for 12 h
Define: AKIN Stage 3
SCr > 3x baseline, >4 mg/dL with acute increase of 0.5 mg/dL, or requiring dialysis OR UOP <0.3mL/kg/h x24 h or anuria for >12h
What urine sediment would be found in pre-renal AKI?
hyaline cast, may also be normal
What urine sediment would be found in intrinsic AKI?
granular casts, cellular debris
What urine sediment would be found in post-renal AKI?
cellular debris
How can AKI be diagnosed?
-fractional excretion of sodium (FENa): urinary excretion of sodium
-fractional excretion of urea (FEUrea): used on patients on diuretics
-renal ultrasound
-urinalysis
-renal biopsy
Goals of therapy: AKI
-minimize ongoing insult
-reduce risk for complications
-expedite and restore baseline function
What are the causes of Pre-Renal AKI?
hypoperfusion to the kidneys
-volume loss such as dehydration, bleeding, or burns
-decreased effective blood volume such as cardiac output, sepsis, or liver failure
-functional such as DRUGS= NSAIDS, ACE Inhibitors, ARBs, diuretics
What is the treatment for Pre-Renal AKI?
-stop offending agents if possible
-fluid replacement (normal saline)
-hemodynamic support (improve utilization of blood volume, vasopressors)
What are the causes of Intrinsic AKI?
structural injury
-tubular injury: acute tubular necrosis (ATN)
-interstitial injury: acute interstitial nephritis (AIN)
-glomerular injury
-vascular injury
What is the most common cause of intrinsic AKI?
acute tubular necrosis (ATN)
What are the causes of acute tubular necrosis (ATN)?
prolonged pre-renal AKI, drugs, or endogenous toxins
What is the treatment for acute tubular necrosis (ANT)?
-stop offending agents
-manage electrolyte imbalances
-possibly diuretics with significant volume overload (furosemide)
-renal replacement therapy (RRT)= dialysis
How can acute tubular necrosis (ATN) be prevented?
recognize high-risk patients such as recent surgery/trauma or drugs and encourage appropriate fluid intake especially with nephrotoxic medications
How is Contrast Induced Nephropathy (CIN) AKI diagnosed?
SCr rise of 0.5+ or 25% increase in baseline within 48h of contrast
What patients are high risk for contrast induced nephropathy (CIN)?
-pre-existing kidney diagnosis
-diabetic nephropathy
-age >70yo
-hypovolemia, hypotension
-anemia
-heart failure
-concomitant nephrotoxins
-large contrast doses, high-osmolality contrast
How can contrast induced nephropathy(CIN) be prevented?
IV volume expansion, PO N-Acetylcystine (NAC) (controversial), ascorbic acid, or remove nephrotoxins and increase monitoring