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Clinical 2 (Sam) > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A

Abrupt (within 48 hours) reduction in kidney function (GFR)

  • loss of excretory function in the kidneys
  • accumulation of metabolic waste products (rapid rise in serum creatinine and urea - azotemia)
  • decreased urine output may occur
  • reduced ability to maintain fluid, electrolyte and acid-base balance
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2
Q

AKI:

Classified in 3 stages based on what?

A
  • Change in serum creatinine level
  • Change in urine output
  • Need for renal replacement therapy
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3
Q

What are some limitations with classifying AKI ?

A
  • Baseline SCr
  • SCr varies with age, gender, muscle mass, diet and hydration
  • [SCr] increase with volume depletion
  • Lag in increased SCr with decreased GFR
  • Urine output may not be reduced (varies with volume status, diuretic administration and presence of obstruction)
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4
Q

When is SCr considered constant?

A

Change in SCr of less than 10-15% within 24h considered “constant”
-SCr level is not a steady state and continues to fluctuate

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5
Q

List the 3 classifications of AKI based on daily urine production

A

Anuric
Oliguric
Nonoliguric

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6
Q

< 50 mL/day

A

anuric

usually only in post-renal cause

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7
Q

50-500 mL/day

A

oliguric

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8
Q

> 500 mL/day

A

nonoliguric

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9
Q

List the 4 types of AKI

A

A) Psuedo

1) Pre-renal
2) Intrinsic
3) Post-renal

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10
Q

Describe Pseudo AKI

A
  • no actual decline in renal function

- increase SCr due to other causes

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11
Q

Describe Pre-renal AKI

A
  • decrease blood flow to kidney

- decreases GFR

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12
Q

Describe Intrinsic AKI

A

-structural damage to kidney

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13
Q

Describe Post-renal AKI

A

-obstruction of urine flow

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14
Q

If obstruction _____ bladder, must involve both kidneys to cause AKI

A

above

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15
Q

_____ kidney injury: elevated creatinine without change in GFR or renal damage

A

Pseudo

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16
Q

Which 2 drugs will cause inhibition of renal tubular secretion of SCr?

A
  • Trimethoprim
  • Cimetidine
  • Will appear to decrease CrCl (measured or estimated)
  • No change in urea
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17
Q

What is the most common cause of AKI?

A

Pre-renal/functional causes

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18
Q

Pre-renal:
Impaired renal blood flow due to?

(3 reasons)

A

1) Intravascular volume depletion
- Dehydration, blood loss, GI loss (diarrhea, vomiting), diuretics, extensive burns

2) Reduced effective blood volume/arterial pressure
- Advanced Liver Disease
- Congestive Heart Failure (decreased cardiac output)
- Hypotension (Antihypertensives)
- Sepsis (systemic vasodilation)

3) Decreased pressure in glomerulus (functional)
- Afferent arteriole vasoconstriction (cyclosporine, tacrolimus, NSAIDs, COX 2 inhibitors, hepatorenal syndrome)
- Efferent arteriole vasodilation (ACEi, ARBs)

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19
Q

What are agents that impair renal blood flow?

A
  • Afferent arteriole vasoconstriction (cyclosporine, tacrolimus, NSAIDs, COX 2 inhibits, hepatorenal syndrome)
  • Efferent arteriole vasodilation (ACEi, ARBs)
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20
Q

What are possible causes of pre-renal AKI?

A

-Dehydration, volume depleted, reduced intake, vomiting, NSAID, ARB use

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21
Q

Describe afferent/efferent effects

A
  • Afferent arteriole will dilate (PG)
  • Efferent arteriole will constrict (Angiotensin 2)
  • Trying to increase pressure
  • ARB or NSAID will inhibit this and then reduce pressure
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22
Q

What are 4 things that affect intrinsic AKI?

A
  • Tubular
  • Vascular
  • Interstitial
  • Glomerular
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23
Q

List 3 types of Intrinsic AKI ?

A

1) Acute Tubular Necrosis (ATN)
2) Acute Interstitial Nephritis
3) Glomerulonephritis (uncommon)

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24
Q

3 Types of Intrinsic AKI

Describe
1) Acute Tubular Necrosis (ATN)

A
  • Ischemia in kidney producing cell damage or direct tubule toxins
  • Medication induced causes: Aminoglycosides, Amphotericin B, Contrast dye
  • Other: Rhabdomyolysis, ethylene glycol
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25
Q

3 Types of Intrinsic AKI

Describe
2) Acute Intersitital Nephritis

A
  • Inflammatory disorder of the renal interstitial (allergic reaction)
  • 2 most common causes: Drugs (penicillins, cephalosporins, loop diuretics, NSAIDs, allopurinol), and infections

Presentation: fever, rash, eosinophilia

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26
Q

3 Types of Intrinsic AKI

Describe
3) Glomerulonephritis (uncommon)

A

-Results from stimulation of the immune system leading to inflammation of the glomerulus

Causes:

  • DNA, patients, viruses, and bacteria stimulate immune activation
  • Ex. SLE (lupus nephritis), post-strep infection glomerulonephritis
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27
Q

Describe Acute Tubular Necrosis caused by Aminoglycosides

A

Gentamicin > Tobramycin > Amikacin

Mechanism:

  • Primarily a direct toxic effect to tubular epithelial cell
  • Accumulation of drug in proximal tubule cells produces necrosis which decreases GFR

Reversible if you D/C drug

28
Q

What are patient specific risk factors for ATN caused by aminoglycosides?

A
  • elderly
  • hypotension
  • volume depletion
  • shock, liver failure
  • chronic renal insufficiency
29
Q

What are drug-regimen risk factors for ATN caused by aminoglycosides?

A
  • large total cumulative dose
  • frequent dosing interval
  • high trough levels > 2 mg/L
  • Duration > 5-7 days
  • Other nephrotoxic agents
30
Q

Describe the presentation of ATN caused by aminoglycosides?

A
  • Nonoliguric (>500 mL/day)
  • Granular casts in urine
  • Increase urea and Sir day 5-10
  • Increase SCr may occur earlier in presence of dehydration, sepsis, hypotension, CHF, concurrent use with other nephrotoxins
31
Q

Prevention of ATN caused by aminoglycosides?

A
  • Avoid in high risk patients
  • Maintain adequate hydration
  • Monitor Sir every 2-4 days
  • Monitor amino glycoside levels and adjust dose for renal function
  • Extended-interval (once-daily) dosing
  • Limit duration of treatment (<7 days)
32
Q

___________ = reversible

A

nephrotoxicity

33
Q

___________ = not reversible

A

ototoxicity

34
Q

What are some post-renal causes?

A
  • Kidney stones
  • Prostate enlargement or cancer
  • Bladder tumor or obstruction
  • Urethral stricture/tumor
  • Crystal deposition in renal tubules (Acyclovir, methotrexate, foscarnet, indinavir, sulfadiazine)
35
Q

Describe the assessment of AKI

A
  • History
  • Acute vs Chronic
  • Baseline SCr and urea
  • Past medical history, family history
  • Other medical conditions (diabetes, poorly controlled hypertension)
  • Med history (functional & intrinsic Aki often drug-induced)
  • Discontinue any meds with potential to cause AKI (esp NSAIDs, COX 2, ACEi/ARB)
36
Q

Describe the clinical presentation of AKI

A

Non-specific:

  • Elevated SCr and urea
  • Decreased urine output
  • Uremic symptoms - weakness, fatigue, N/V, loss of appetite, mental confusion, asterixis, seizures

*uremic symptoms due to build up of nitrogenous waste (not actual urea)

37
Q

Asterixis

A

hand flap

38
Q

look at chart on page 6

A

okay

39
Q

Signs of hypovolemia

A
  • orthostatic hypotension
  • hands and feet cool to touch
  • dry oral mucosa
  • poor skin turgor
40
Q

Describe Prerenal Investigations

A
  • Renal response to decreased perfusion is to increase resorption of salt and water
  • Kidneys recognize decreased perfusion as a low BP state and work towards improving BP
  • Passively, urea resorption is also increased in the proximal tubule
  • Creatinine resorption is not affected by renal perfusion
  • This results in increased serum urea/creatinine, lower urinary Na, lower FeNa
41
Q

Normal Urea/Cr ratio

A

70

42
Q

Urea/Cr ratio that indicates pre-renal AKI

A

> 70

43
Q

Urea/Cr ratio that indicates intrinsic AKI

A

<70

44
Q

Urine Na that indicates pre-renal AKI

A

<20

45
Q

Urine Na that indicates intrinsic AKI

A

> 40

46
Q

FENa that indicates pre-renal AKI

A

<1%

47
Q

FENa that indicates intrinsic AKI

A

> 2%

48
Q

_____ in urine is elevated in CKD

A

protein

49
Q

What do RBC casts cause?

A

glomerulonephritis

50
Q

What do WBC casts cause?

A

acute interstitial nephritis, pyelonephritis

51
Q

Crystals in urine mean ?

A

may suggest kidney stone/post-renal obstruction

52
Q

Eosinophils in urine mean ?

A

acute interstitial nephritis

53
Q

Protein in urine mean ?

A
  • intrinsic renal disease with glomerular damage

- may investigate further using 24 hour urine collection

54
Q

Hematuria in urine mean ?

A
  • acute intrinsic injury

- glomerulonephritis

55
Q

Coarse, granular “muddy brown” casts cause ?

A

ATN (acute tubular nephritis)

56
Q

High osmolarity = ?

> 500 mOsm/L

A

pre-renal AKI

57
Q

Low osmolarity = ?

<350 mOsm/L

A

intrinsic damage

-structural damage unable to concentrate

58
Q

Goals of therapy of AKI

A

1) Minimize kidney injury
- Remove cause - discontinue nephrotoxic agents)

2) Supportive therapy
- Fluid, electrolyte, nutritional support
- Possible renal replacement therapy
- Treat non-renal complications (sepsis, GI bleed)

3) Restore renal function to baseline
- Usually takes 10-14 days from resolution of last insult

59
Q

What is the treatment for pre-renal/functional AKI?

A

-Hydrate to increase BP and GFR
OR
-Treat underlying disorder (blood loss, sepsis, CHF, diarrhea/vomitting)
AND
-D/C common med causes (NSAID/Cox 2 inhibitors, ACEi/ARB) until cause of AKI determined
-D/C diuretics in CHF and cirrhosis
-D/C antihypertensives if hypotensive

60
Q

What is the treatment for intrinsic AKI?

A

Intrinsic Causes:

a) Acute Tubular Necrosis (ATN)
- No specific treatment
- Manage complications

b) Acute Interstitial Nephritis (drug-induced)
- Withdraw precipitation drug
- Consider steroid therapy

c) Glomerulonephritis
- Depends on cause

61
Q

What is the treatment for post-renal AKI ?

A

Urology consult:

  • Catheter if obstruction at bladder or below
  • Nephrostomy tubes if obstruction above bladder

For drug-induced crystal nephropathy:

  • D/C med if possible
  • IV fluids to ensure adequate hydration
  • Methotrexate (alkalinize urine with IV or oral sodium bicarbonate)
62
Q

What are some AKI complications?

A
  • Fluid overload (can lead to pulmonary deem)

- Hyperkalemia (can lead to cardiac arrhythmias)

63
Q

What are some reasons for diuretic resistance?

A
  • excessive sodium intake
  • decreased GFR and functioning nephrons (ATN)
  • failure to reach site of action
  • distal tubule cells hypertrophy to reabsorb more Na
64
Q

Indications for renal replacement therapy?

AEIOU

A

Acid-base abnormalities
-metabolic acidosis from accumulation of organic/inorganic acids

Electrolyte imbalance
-hyperkalemia, hypermagnesemia

Intoxications
-salicylates, lithium

Fluid Overload (resistant to diuretics)

Uremia (severe/smptomatic)

65
Q

What are uremia symptoms?

A

mental confusion, asterixis, seizures

66
Q

What is renal replacement therapy?

A
  • Intermittent Hemodialysis (Most frequently used for chronic renal failure)
  • Continuous Renal Replacement Therapies

Clinical 2 (Sam) (18 decks)

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