Exam 3 - Acute Kidney Injury Flashcards

1
Q

What is the general criteria for diagnosis of AKI based on?

A

Usually based on serum creatinine levels OR decrease in a patientโ€™s urine output

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2
Q

What is the KDIGO Diagnostic criteria for AKI?

A
  • Increase in serum creatinine by > or equal to 0.3 mL/dL within 48 hours
    OR
  • Increase in serum creatinine > or equal to 1.5 times baseline
    OR
  • Urine volume < 0.5 mL/kg/hour for six hours
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3
Q

What is the KDIGO staging and associated Cr levels?

A

Stage 1: Increase in serum Cr to 1.5-1.9 times baseline
Stage 2: Increase in serum Cr to 2.0-2.9 times baseline
Stage 3: Increase in serum Cr to 3.0 times baseline OR anuria for > 12 hours OR initiation of renal replacement therapy

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4
Q

What are the classifications of AKI etiology?

A
  • Prerenal: decreased renal perfusion
  • Intrinsic renal: pathology of the vessels, glomeruli, or tubules
  • Postrenal: obstructive
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5
Q

What is AKI in the hospital most often from?

A
  • Prerenal

- Intrinsic

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6
Q

What is the most common AKI etiology?

A

ATN (intrinsic)

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7
Q

What are major causes of prerenal disease?

A
  • True volume depletion
  • Hypotension
  • Edematous states
  • Selective renal ischemia
  • Drugs affecting GFR
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8
Q

What are major causes of intrinsic renal disease?

A
  • Renal ischemia
  • Sepsis
  • Nephrotoxins (IV contrast)
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9
Q

How is ATN caused by IV contrast?

A

IV contrast causes renal tubular epithelial cell toxicity and renal medullary ischemia from vasoconstriction

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10
Q

What are risk factors for developing ATN from IV contrast?

A
  • Preexisting renal disease
  • Volume depletion
  • Repeated doses of contrast
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11
Q

How can you avoid ATN caused by IV contrast?

A
  • Hydration
  • Use of low-osmolal agents at low doses
  • Avoid repetitive doses
  • Avoidance of nephrotoxic drugs for at least 48 hours after exposure (Metformin, NSAIDs)
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12
Q

A reduction in GFR in patients without intrinsic renal disease requires what type of obstruction?

A

Requires bilateral obstruction, or unilateral obstruction if single functioning kidney

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13
Q

What urine output levels differentiate oliguric from anuric?

A

Oliguric: < 400 mL/24 hours

Anuric: < 50 to 100 mL/24 hours

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14
Q

Muddy brown casts on UA are pathognomonic for what?

A

ATN (intrinsic)

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15
Q

What equation/calculation can help distinguish prerenal AKI from intrinsic ATN?

A

FENa (fractional excretion of sodium)

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16
Q

If the FENa is <1%, what does this suggest?

If the FENa is >2%, what does this suggest?

A

<1% suggests prerenal

> 2% suggests intrinsic (ATN)

  • **between 1-2% can be seen with either disorder
  • **unreliable in patients taking diuretics
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17
Q

What are some pearls/pitfalls to note with using FENa as a tool?

A
  • Unreliable for patients on diuretics

- Serum creatine is not stable in AKI

18
Q

When is renal imaging typically performed and what is a major reason for doing it?

A

Generally performed in patients with AKI when the underlying cause is not immediately apparent

Major reason is to assess for urinary tract obstruction

19
Q

What is the most common radiographic technique for AKI?

A

Renal ultrasound

20
Q

When is a renal biopsy done?

A

Rarely, but in those who have no clear explanation for AKI.

If creatinine is markedly elevated or if it significantly worsens over the course of days

21
Q

What are some contraindications to a renal biopsy?

A
  • Bleeding diathesis
  • Severe HTN
  • Pyelonephritis
  • Renal tumor
  • Solitary native kidney
22
Q

While many patients have mild AKI, what life-threatening complications can occur?

A
  • Volume imbalance (depletion or overload)
  • Metabolic acidosis (pH < 7.4)
  • Hyperkalemia (K+ > 5.5)
  • Hypocalcemia
  • Hyperphosphatemia
  • Uremia
23
Q

If patient with AKI presents with history and exam consistent with volume depletion, and/or has oliguria, what should you do?

A

Administer IV crystalloid isotonic fluids (0.9 NS)

Begin wtih 1-3 liters of fluid and performed repeated assessments

24
Q

If patient with AKI presents with clinical signs of volume depletion and you treat with IV fluids but they do not respond, what does this suggest?

A

Unlikely to have prerenal disease and more likely to have ATN or other forms of instrinsic AKI

25
What can fluid overload/retention lead to if not treated?
Pulmonary edema
26
How should you treat a fluid overloaded patient with AKI?
Diuretics if patient not anuric, BUT - should not be prolonged therapy - UOP should be monitored and if it does not increase, diuretics should be stopped and alternate therapy such as dialysis should be started
27
Why does metabolic acidosis occur in AKI?
- The excretion of acid and regeneration of bicarbonate is impaired with a low GFR - Many causes of AKI produce increased amounts of acid
28
What is the treatment for metabolic acidosis in AKI?
- Dialysis | - Bicarb administration
29
In the treatment of metabolic acidosis in AKI, when would dialysis be preferred over bicarbonate?
Dialysis is preferred for those who are oligo-anuric and/or volume overloaded as bicarb administration results in large sodium load that can contribute to overload
30
In the treatment of metabolic acidosis in AKI, when would bicarbonate be preferred over dialysis?
If not volume overloaded and no other indication for dialysis especially if - Acidosis is related to diarrhea - pH < 7.1 and awaiting dialysis
31
What are two significant abnormalities that hyperkalemia can cause?
- Impaired neuromuscular transmission | - Cardiac conduction abnormalities (arrhythmias)
32
What is the treatment for hyperkalemia in AKI?
Both medical therapy and dialysis
33
What is hypocalcemia primarily related to in AKI?
Primarily related to increases in serum phosphorus levels caused by reduced GFR (inverse relationship)
34
How should you treat symptomatic hypocalcemic patients versus asymptomatic?
Symptomatic: - IV calcium Asymptomatic: - Correct hyperphosphatemia first
35
What are some symptoms associated with hypocalcemia?
- Paresthesias - Tetany - Confusion - Seizures - Trousseau's sign - Chvostek's sign - QT prolongation
36
What constitutes moderately-severely elevated serum phosphate levels (hyperphosphatemia) and how should it be treated?
Serum phosphate levels > 5.5 Treated with dietary phosphate binders (depends on calcium concentration)
37
If levels of serum ionized calcium concentration are low, what phosphate binder should be given to treat hyperphosphatemia? What if levels are high?
Low: Calcium acetate or calcium carbonate High: Aluminum hydroxide or lanthanum carbonate
38
What does uremia mean?
Urine in the blood
39
How do you treat severe uremia?
Dialysis
40
What is the most common cause of obstruction Of the urinary tract (postrenal)?
- Prostatic disease (hyperplasia or cancer) | - Metastatic cancer