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Clinical Med II > Exam 3 - Acute Kidney Injury > Flashcards

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 patient’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
Q

What can fluid overload/retention lead to if not treated?

A

Pulmonary edema

26
Q

How should you treat a fluid overloaded patient with AKI?

A

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
Q

Why does metabolic acidosis occur in AKI?

A
  • The excretion of acid and regeneration of bicarbonate is impaired with a low GFR
  • Many causes of AKI produce increased amounts of acid
28
Q

What is the treatment for metabolic acidosis in AKI?

A
  • Dialysis

- Bicarb administration

29
Q

In the treatment of metabolic acidosis in AKI, when would dialysis be preferred over bicarbonate?

A

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
Q

In the treatment of metabolic acidosis in AKI, when would bicarbonate be preferred over dialysis?

A

If not volume overloaded and no other indication for dialysis especially if

  • Acidosis is related to diarrhea
  • pH < 7.1 and awaiting dialysis
31
Q

What are two significant abnormalities that hyperkalemia can cause?

A
  • Impaired neuromuscular transmission

- Cardiac conduction abnormalities (arrhythmias)

32
Q

What is the treatment for hyperkalemia in AKI?

A

Both medical therapy and dialysis

33
Q

What is hypocalcemia primarily related to in AKI?

A

Primarily related to increases in serum phosphorus levels caused by reduced GFR (inverse relationship)

34
Q

How should you treat symptomatic hypocalcemic patients versus asymptomatic?

A

Symptomatic:
- IV calcium

Asymptomatic:
- Correct hyperphosphatemia first

35
Q

What are some symptoms associated with hypocalcemia?

A
  • Paresthesias
  • Tetany
  • Confusion
  • Seizures
  • Trousseau’s sign
  • Chvostek’s sign
  • QT prolongation
36
Q

What constitutes moderately-severely elevated serum phosphate levels (hyperphosphatemia) and how should it be treated?

A

Serum phosphate levels > 5.5

Treated with dietary phosphate binders (depends on calcium concentration)

37
Q

If levels of serum ionized calcium concentration are low, what phosphate binder should be given to treat hyperphosphatemia?

What if levels are high?

A

Low: Calcium acetate or calcium carbonate

High: Aluminum hydroxide or lanthanum carbonate

38
Q

What does uremia mean?

A

Urine in the blood

39
Q

How do you treat severe uremia?

A

Dialysis

40
Q

What is the most common cause of obstruction Of the urinary tract (postrenal)?

A
  • Prostatic disease (hyperplasia or cancer)

- Metastatic cancer

Clinical Med II (17 decks)

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