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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
3 Types of Intrinsic AKI Describe 2) Acute Intersitital Nephritis
- 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
26
3 Types of Intrinsic AKI Describe 3) Glomerulonephritis (uncommon)
-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
27
Describe Acute Tubular Necrosis caused by Aminoglycosides
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
What are patient specific risk factors for ATN caused by aminoglycosides?
- elderly - hypotension - volume depletion - shock, liver failure - chronic renal insufficiency
29
What are drug-regimen risk factors for ATN caused by aminoglycosides?
- large total cumulative dose - frequent dosing interval - high trough levels > 2 mg/L - Duration > 5-7 days - Other nephrotoxic agents
30
Describe the presentation of ATN caused by aminoglycosides?
- 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
Prevention of ATN caused by aminoglycosides?
- 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
___________ = reversible
nephrotoxicity
33
___________ = not reversible
ototoxicity
34
What are some post-renal causes?
- Kidney stones - Prostate enlargement or cancer - Bladder tumor or obstruction - Urethral stricture/tumor - Crystal deposition in renal tubules (Acyclovir, methotrexate, foscarnet, indinavir, sulfadiazine)
35
Describe the assessment of AKI
- 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
Describe the clinical presentation of AKI
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
Asterixis
hand flap
38
look at chart on page 6
okay
39
Signs of hypovolemia
- orthostatic hypotension - hands and feet cool to touch - dry oral mucosa - poor skin turgor
40
Describe Prerenal Investigations
- 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
Normal Urea/Cr ratio
70
42
Urea/Cr ratio that indicates pre-renal AKI
>70
43
Urea/Cr ratio that indicates intrinsic AKI
<70
44
Urine Na that indicates pre-renal AKI
<20
45
Urine Na that indicates intrinsic AKI
>40
46
FENa that indicates pre-renal AKI
<1%
47
FENa that indicates intrinsic AKI
>2%
48
_____ in urine is elevated in CKD
protein
49
What do RBC casts cause?
glomerulonephritis
50
What do WBC casts cause?
acute interstitial nephritis, pyelonephritis
51
Crystals in urine mean ?
may suggest kidney stone/post-renal obstruction
52
Eosinophils in urine mean ?
acute interstitial nephritis
53
Protein in urine mean ?
- intrinsic renal disease with glomerular damage | - may investigate further using 24 hour urine collection
54
Hematuria in urine mean ?
- acute intrinsic injury | - glomerulonephritis
55
Coarse, granular "muddy brown" casts cause ?
ATN (acute tubular nephritis)
56
High osmolarity = ? | > 500 mOsm/L
pre-renal AKI
57
Low osmolarity = ? | <350 mOsm/L
intrinsic damage | -structural damage unable to concentrate
58
Goals of therapy of AKI
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
What is the treatment for pre-renal/functional AKI?
-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
What is the treatment for intrinsic AKI?
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
What is the treatment for post-renal AKI ?
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
What are some AKI complications?
- Fluid overload (can lead to pulmonary deem) | - Hyperkalemia (can lead to cardiac arrhythmias)
63
What are some reasons for diuretic resistance?
- excessive sodium intake - decreased GFR and functioning nephrons (ATN) - failure to reach site of action - distal tubule cells hypertrophy to reabsorb more Na
64
Indications for renal replacement therapy? | AEIOU
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
What are uremia symptoms?
mental confusion, asterixis, seizures
66
What is renal replacement therapy?
- Intermittent Hemodialysis (Most frequently used for chronic renal failure) - Continuous Renal Replacement Therapies

Clinical 2 (Sam) (18 decks)

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