Acute Kidney Injury (AKI) Flashcards

1
Q

Define: Acute Kidney Injury

A

acute worsening in renal function

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2
Q

Define: Oliguria

A

urine output (UOP) < 500 mL/day

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3
Q

Define: Anuria

A

urine output (UOP) < 50 mL/day

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4
Q

What are the risk factors of AKI?

A

-sepsis/critical illness
-dehydration
-burns
-trauma
-surgery
-nephrotoxic drugs
-contrast agents
-advanced age
-female gender
-CKD
-diabetes
-cancer

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5
Q

KDIGO AKI DEFINITION

A

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

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6
Q

RIFLE CRITERIA

A

-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

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7
Q

Define: AKIN Stage 1

A

SCr increase 0.3 mg/dL or 1.5-2x baseline OR UOP <0.5mL/kg/h in 6h

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8
Q

Define: AKIN Stage 2

A

SCr increase 2-3x baseline OR UOP <0.5 mL/kg/h for 12 h

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9
Q

Define: AKIN Stage 3

A

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

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10
Q

What urine sediment would be found in pre-renal AKI?

A

hyaline cast, may also be normal

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11
Q

What urine sediment would be found in intrinsic AKI?

A

granular casts, cellular debris

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12
Q

What urine sediment would be found in post-renal AKI?

A

cellular debris

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13
Q

How can AKI be diagnosed?

A

-fractional excretion of sodium (FENa): urinary excretion of sodium
-fractional excretion of urea (FEUrea): used on patients on diuretics
-renal ultrasound
-urinalysis
-renal biopsy

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14
Q

Goals of therapy: AKI

A

-minimize ongoing insult
-reduce risk for complications
-expedite and restore baseline function

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15
Q

What are the causes of Pre-Renal AKI?

A

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

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16
Q

What is the treatment for Pre-Renal AKI?

A

-stop offending agents if possible
-fluid replacement (normal saline)
-hemodynamic support (improve utilization of blood volume, vasopressors)

17
Q

What are the causes of Intrinsic AKI?

A

structural injury
-tubular injury: acute tubular necrosis (ATN)
-interstitial injury: acute interstitial nephritis (AIN)
-glomerular injury
-vascular injury

18
Q

What is the most common cause of intrinsic AKI?

A

acute tubular necrosis (ATN)

19
Q

What are the causes of acute tubular necrosis (ATN)?

A

prolonged pre-renal AKI, drugs, or endogenous toxins

20
Q

What is the treatment for acute tubular necrosis (ANT)?

A

-stop offending agents
-manage electrolyte imbalances
-possibly diuretics with significant volume overload (furosemide)
-renal replacement therapy (RRT)= dialysis

21
Q

How can acute tubular necrosis (ATN) be prevented?

A

recognize high-risk patients such as recent surgery/trauma or drugs and encourage appropriate fluid intake especially with nephrotoxic medications

22
Q

How is Contrast Induced Nephropathy (CIN) AKI diagnosed?

A

SCr rise of 0.5+ or 25% increase in baseline within 48h of contrast

23
Q

What patients are high risk for contrast induced nephropathy (CIN)?

A

-pre-existing kidney diagnosis
-diabetic nephropathy
-age >70yo
-hypovolemia, hypotension
-anemia
-heart failure
-concomitant nephrotoxins
-large contrast doses, high-osmolality contrast

24
Q

How can contrast induced nephropathy(CIN) be prevented?

A

IV volume expansion, PO N-Acetylcystine (NAC) (controversial), ascorbic acid, or remove nephrotoxins and increase monitoring

25
Q

What are the causes of acute interstitial nephritis (AIN)?

A

inflammation of interstitium around tubules
most commonly drug induced (antibiotics= beta-lactams, sulfa, COX-2, NSAIDS, loop diuretics, PPI or H2RAs (usually 2 weeks within exposure)) but other causes include infection, connective tissue disease, exogenous toxins

26
Q

What is the treatment of acute interstitial nephritis (AIN)?

A

-stop offending agent
-treat underlying cause
-if no significant improvement -> corticoidsteroids

27
Q

What are the causes of Post-Renal AKI?

A

obstruction
-physical blockage
-improper placement of urinary catheter
-crystal formation
-drugs: sulfonamides (antibiotics), antiretrovirals (HIV), methotrexate, acyclovir

28
Q

What is the treatment for Post-Renal AKI?

A

-remove/relieve obstruction
-stop offending agents
-aggressive hydration
-potential for urine alkalinization if certain drugs are involved

29
Q

What are the indications for renal replacement therapy (RRT)?

A

life threatening changes in fluids, electrolytes, or acid-base status
-A= acid/base
-E= electrolyte abnormalities
-I= intoxicants
-O= volume overload
-U= uremia

30
Q

What monitoring parameters should be put in place for a patient with AKI?

A

-body weight
-fluid intake and output
-signs and symptoms of edema or dehydration
-BP
-serum electrolytes
-ab markers of renal function= SCr and BUN

31
Q

What are the complications of AKI?

A

-METABOLIC: electrolyte imbalances, acid/base disorders, accumulation of toxins
-CARDIOVASCULAR: edema, hypertension, arrhythmias
-hematologic: platelet dysfunction
-development of CKD