Acute Kidney Injury Flashcards

1
Q

Lab definition of AKI

A

1) SCr bump by 0.3 mg/dL
2) Scr bump by 50%
3) UOP <0.5mL/kg.hr

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2
Q

Stage I AKI

A

1.0- to 1.5-fold increase in SCr, or decline in UOP to 0.5 mL/kg/h over 6–12 hours

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3
Q

Stage II AKI

A

2.0- to 2.9-fold increase in SCr or decline in UOP to 0.5 mL/kg/h over 12 hours or longer

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4
Q

Stage III AKI

A

3-fold or greater increase in SCr or decline in UOP to less than 0.3 mL/kg/h for 24 hours or longer or anuria for 12 hours or longer

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5
Q

Signs and sxs of AKI due to ____, or underlying.

A
  1. Uremia - N/V, malaise, altered sensorium, +/- asterixsi
  2. HTN, fluidoverload
  3. Pericardial effusion/tamponade +/- friction rub
  4. Arrhythmia (hyperkalemia)
  5. Coagulopathy - platelet dysfunction from uremia
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6
Q

Lab findings in AKI

A

BMP - high SCr, BUN, K
Ph - high
AG and non-gap metabolic acidosis

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7
Q

Categories of AKI

A
  1. pre-renal
  2. intrinsic
  3. post-renal
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8
Q

Pre-renal causes of AKI

A
  1. Poor renal perfusion – hypovolemia, decreased cardiac output, systemic vasodilation (sepsis), acute/chronic anemia, burns, GI losses, overdiuresis
  2. Renal vasoconstriction - NSAIDS, ACEi/ARBs, contrast, calcineurin inhibitors, HRS, hyperCa
  3. Large vessel - RAS, vasculitis, dissection, abd compartment syndrome, renal venous congestion, VTE
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9
Q

Urinalysysis in pre-renal

A
  1. Bland sediment, hyaline casts (nonspecific)
  2. FeNa <1%
  3. UNa <20
  4. Uosm >500
  5. BUN:Cr >20
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10
Q

Post-renal causes of AKI

A
  1. urethral obstruction, bladder dysfunction/obstruction, ureteral obstruction, BPH, anticholinergic meds, malignancy to bladder/prostate/cervix, retroperitoneal fibrosis, neurogenic bladder
  2. Less common: blood clots, bilateral ureteral stones, urethral stones/stricture, bilaterally papillary necrosis
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11
Q

Urinalysis in post-renal

A
  1. May appear to be prerenal at first

2. Bland sediment, variable FeNa

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12
Q

Intrinsic causes of AKI

A
  1. Acute Tubular Necrosis
  2. Acute Interstitial nephritis
  3. Small-med vasculitis
  4. Glomerulonephritis
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13
Q

Etiologies of ATN

A
  1. Ischemia - progression on inadequately treated prerenal
  2. Toxins
  3. Contrast-induced
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14
Q

Common toxins leading to ATN

A

aminoglycosides, amphotericin B, cisplatin, HES

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15
Q

What two preexisting conditions predispose a patient the greatest for CIAKI (contrast-induced AKI)

A

Renal insufficiency (SCr >2.0 and DM)

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16
Q

Timeline of CIAKI

A
  1. AKI within 24-48 hours after the radiocontrast study
  2. Peak 3-5 days
  3. Resolves 7-10 days
17
Q

Lab work-up in ATN

A

BMP: hyperkalemia, BUN:Cr <20:1
Ph elevated
FeNa >2%
UA: muddy brown casts

18
Q

Three phases of ATN

A
  1. Initial injury
  2. Maintenance - oliguric vs nonoliguric, 1-3 weeks to several months of cellular repair and removal of tubular debris
  3. Recovery - heralded by diuresis
19
Q

Signs / sxs of AIN

A

Fever
Transient maculopapular rash
Pyuria with eosinophilia, WBC casts, hematuria