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Nephrology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Risk factors for acute kidney injury

8

A
  1. Age > 75
  2. DM
  3. Preexisting chronic kidney disease
  4. CHF
  5. Liver failure
  6. Sepsis
  7. Exposure to IV contrast
  8. Cardiac surgery
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2
Q

Acute kidney injury definition

3 components

A

Abrupt (within 48 hours) decline in kidney function as manifested by
1. Increase in serum creatinine
≥ 0.3 mg/dL or ≥ 1.5 times that from baseline
2. OR decrease in urine output of less than 0.5 mL/kg/hr X 6h
3. OR need for dialysis

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3
Q

What is azotemia? 2

What is Oliguria?

What is Anuria?

A
    • Elevated BUN and/or creatinine
    • The build up of abnormally large amounts of nitrogenous waste products in the blood
  2. Urine output less than 400 mL/day
    Urine output less than 20 cc/hr
  3. Urine output less than 100 mL/day
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4
Q

Can be asymptomatic but when symptoms are present they are secondary to what?

A

uremia/azotemia

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5
Q

What are the symtpoms of acute renal injury?

9

A
  1. Nausea, vomiting
  2. Malaise
  3. Altered sensorium
  4. Hypertension
  5. Pericardial effusion, pericardial friction rub, arrhythmias
  6. Pulmonary edema
  7. Abdominal pain, ileus
  8. Bleeding secondary to platelet dysfunction
  9. Encephalopathic changes including asterixis, confusion, seizures
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6
Q

Where does BUN come from?

5 steps

A
  1. When protein is used for energy the carbon is cleaved from the amino acid and leaves behind a Nitrogren.
  2. The N takes up 3 H+ to form NH3+ which is ammonia.
  3. The ammonia (NH3+) is then processed through the liver to become urea.
  4. When the urea enters the blood stream it is called the blood urea nitrogren (BUN).
  5. The blood urea nitrogren is then excreted by the kidney
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7
Q
  1. Why does BUN increase?

2. What causes elevated BUN levels? 6

A
  1. when protein is broken down and more ammonia forms
    • Burns
    • Tetracycline
    • Steroids
    • Fever
    • Catabolic state
    • GI bleeding
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8
Q

When wil BUN decrease?

A

Liver failure- If the liver is unavailable to convert ammonia to urea then the BUN will decrease and the ammonia increases

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9
Q

Decreased GFR (glomerular filtration rate) leads to increased BUN in 2 ways

A
  1. Decreased flow through the glomerulus

2. Slower transport time allows more BUN to be resorbed at the level of the PCT

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10
Q

What is Creatinine:

  1. How is it formed?
  2. How does muscle mass affect the creatinine?
  3. How does age affect the creatinine?
A
  1. Creatinine is formed from the normal breakdown of muscle
  2. The more muscle mass the higher the creatinine
  3. The lower the muscle mass the lower the creatinine (therefore normal reduction in creatinine as a person ages and loses muscle mass)
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11
Q
  1. Decreased GFR leads to what?
  2. How is creatinine handled differently by the kidney?
  3. What happens to it in the DCT?
  4. What drugs will block this from happening in the DCT? 2
A
  1. Decreased GFR also leads to increased creatinine
  2. Instead of the creatinine being reabsorbed in the tubules like BUN…. with a decreased GFR the creatinine is just dumped out
  3. In the DCT creatinine is actively secreted from the body to be eliminated by the kidneys

4.

  1. cimetidine and
  2. trimethoprim therefore increasing the serum creatinine
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12
Q

Causes of Increased BUN?

4

A
  1. Decreased GFR
  2. Less BUN presented at the glomerulus to be removed from the blood
  3. Slower transport time through 4. PCT allows more reabsorption
    Increased protein breakdown
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13
Q

Increased Creatinine?

A
  1. Increased with muscle breakdown
  2. Blockage at the sites in the DCT that allow for active secretion
  3. Decreased GFR as there is less creatinine presented at the glomerulus to be filtered out
    (not reabsorbed in the PCT like BUN)
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14
Q

Normal BUN/creatinine levels?

What kind of state does it occur in?

A

Normal is 10-20:1
Elevated is > 20:1
Increased ratio in a low flow (low blood pressure) state

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15
Q

Laboratory abnormalities with AKI

8

A
  1. Increased BUN, Creatinine
  2. Decreased GFR
  3. Hyperkalemia
  4. Hypocalcemia
  5. Hyperphosphatemia
  6. Anemia
    7, Platelet dysfunction
  7. Anion gap metabolic acidosis
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16
Q

Classification of acute kidney injury is based on where the problem lies.
3 classifications?

A
  1. Prerenal (decreased renal perfusion)
  2. Intrinsic (alteration of normal process within the kidney)
  3. Post renal (inadequate drainage of urine distal to the kidney)
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17
Q

The problem with prerenal failure is what?

A

lack of blood flow to the glomerulus

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18
Q

Prerenal failure can occur with the following disease processes?
7

A
  1. Low cardiac output (CHF)
  2. Hypotension (shock, sepsis, CHF)
  3. Hypovolemia (bleeding, vomiting, diarrhea, etc)
  4. Renal artery stenosis
  5. Renal artery atheroembolic disease
  6. Decreased glomerular perfusion pressure by dilation of the efferent arteriole (ACEI and ARBs)
  7. Decreased glomerular perfusion pressure by dilation of the afferent arteriole by NSAIDs
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19
Q

In an attempt to increase
Volume in a low flow state
Na is reabsorbed. How?

A
  1. Decreased renal perfusion
  2. leads to increase in Angio II and Aldosterone
  3. HCO3 reabsorbtion, H+ secretion and K+ secretion
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20
Q
  1. What does the increased K+ secretion lead to?

2. What does the increased HCO3 reabsorption and H+ secretion lead to?

A
  1. Hypokalemia

2. Metabolic alkalosis (maintance)

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21
Q
  1. Because of low perfusion pressures in prerenal failure the kidney increases what?
  2. What is this an attempt to do?
  3. If this is the case, what would the urine sodium and
  4. urine osmolality (and SG?) be in prerenal failure?
A
  1. Na+ reabsorption
  2. Increase volume
  3. Urine sodium is low
    Urine water content is low which makes it very concentrated =
  4. high osmolality, high specific gravity
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22
Q

Summary of prerenal failure abnormalities
1-2. What is elevated?

3-4. What is low?

  1. What may we see in the urine?
  2. What is the FENa?
A
  1. BUN/creatinine ratio is elevated (>20:1)
  2. elevated SG and osmolality (osmolality > 500; SG > 1.010)
  3. Urine sodium is low (
23
Q

Treatment of prerenal failure
5

Whats the prognosis?

A
  1. Treat underlying cause
  2. Maintain euvolemia
  3. Maintain as near a normal electrolyte status
  4. Avoid nephrotoxic drugs (NSAIDs, glucophage, diuretics, IV contrast, ACEI, ARB, etc)
  5. Short course of dialysis may be needed

The good news…..most recover over time

24
Q

Postrenal failure:

  1. Is it reversible?
  2. How common is it?
  3. What is the cause? 4
  4. What is the most common cause?
A
  1. Reversible
  2. Least common cause of acute kidney injury (5-10%)
  3. Obstruction somewhere in the -kidney,
    - ureter,
    - bladder or
    - urethra
  4. Most common cause is prostatic obstruction
25
Q

Specific disease processes/meds that cause postrenal failure

5

A
  1. BPH (benign prostatic hypertrophy)
  2. Anticholinergic drugs (cause urinary retention)
  3. Cancers (bladder, prostate, cervical)
  4. Neurogenic bladder (spinal cord injury)
  5. Urethral stones or strictures
26
Q

Postrenal signs and symptoms

7

A
  1. History is key
  2. May present with oliguria or anuria
  3. Low back pain or abdominal pain
  4. Flank pain
  5. Enlarged prostate or pelvic mass on exam
  6. Distended bladder
  7. Inability to void
27
Q

Depending on history, work up may include:

4

A
  1. Bladder ultrasound
  2. Bladder catheterization (diagnostic and therapeutic)
  3. CT scan of the abdomen and pelvis (renal stones and hydronephrosis)
  4. Ultrasound of the kidney may show hydronephrosis
28
Q

Abnormalities noted in postrenal failure

  1. BUN/Creatinine ratio?
  2. Urine sodium?
  3. Urine osmolality?
  4. Urin sediment? 4
A
  1. BUN/creatinine ratio 10-20:1
  2. Urine sodium variable depending on the degree of obstruction
  3. Urine osmolality may be high in the beginning and end up less than 400
  4. Urine sediment may be
    - normal,
    - have RBCs,
    - white cells and
    - possibly crystals
29
Q

Treatment of postrenal failure
1. Possibly may relieve obstruction temporarily by what?

  1. Refer to urology for definitive treatment. What are our options here?
    6
A
  1. placement of a bladder catheter
    • Ureteral stent
    • Urethral stent
    • Ureterolithiasis
    • Lithotripsy
    • Nephrostomy tube
    • Prostate resection
30
Q

Intrinsic:
1. Prerenal causes can lead to what? 2

  1. Intrinsic renal failure is what kind of disease?
  2. Sites of injury include? 4
A

Exclude pre and post renal causes (many are reversible)

  1. Prerenal failure that is not treated can lead to ischemia and development of intrinsic failure
  2. Renal parenchymal disease
  3. Sites of injury include
    - glomerulus
    - interstitum
    - tubules
    - vasculature
31
Q

Acute Glomerulonephritis
Pathophysiology?

What kind of diseases cause this? 4

What will you find in the urine? 2

A

Immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.

1. Post streptococcal GN falls in this category
Systemic illnesses
2. SLE
3. Wegeners
4. Goodpastures
    • +Red cell casts and
    • significant proteinuria
32
Q

Acute Interstitial Nephritis

  1. Most cases are related to what?
  2. Also caused by?
  3. 1/3 of the time the pt has a history of what? 3
  4. What will you find in the urine?
A
  1. Most cases related to medication use
  2. Also caused by bacterial, viral or fungal infections of the kidney
  3. 1/3 of the time history of
    - maculopapular rash,
    - fever,
    - arthralgias
  4. Eosinophils in the urine
33
Q

What is the most common type of acute intrinsic renal injury?

A

Acute tubular necrosis

34
Q

What are the three main causes of ATN? 3

A

3 main causes are

  1. ischemia,
  2. sepsis and
  3. nephrotoxic drugs
35
Q

Acute tubular necrosis occurs when what happens?

A

Tubules fail to function

36
Q
  1. Acute tubular necrosis fails to reabsorb what? 3
  2. What will the following levels be:
    - urine sodium?
    - Urine SG?
    - Osmolallity?
    - BUN/Creatinine ratio?
  3. What will we see in the urine?
A
  1. Failure to reabsorb BUN
    Failure to reabsorb sodium and water
    • elevated urine sodium (> 20)
    • low urine SG
    • osmolality less than 450
    • BUN/creatinine ratio should be less than 10:1
  3. Cell sloughing causes the urine to be positive for sediment
  • muddy brown casts (granular),
  • renal tubular epithelial cells and
  • epithelial cell casts
37
Q
  1. ATN secondary to ischemia
    pathophysiology?
    3 contributing factors
A
  1. Tubular damage from site of low perfusion
  2. Inadequate GFR (prerenal) but also by
  3. decreased renal blood flow to the renal cellular functional units
38
Q

What disease processes could cause ATN secondary to ischemia?
5

A
  1. Prolonged hypotension
  2. Hypoxemia
  3. Shock
  4. Sepsis
  5. Prolonged surgery (esp. cardiac and major vascular)
39
Q

ATN secondary to toxins

  1. May occur how many days after exposure?
  2. Drugs that could cause this? 5
  3. Other toxic substances? 1
A
  1. May occur 5-10 days after exposure
  2. Aminoglycosides (up to 25% of patients receiving these drugs)
    - Gentamicin, amikacin (most nephrotoxic)
    - Streptomycin and tobramycin
  3. Amphotericin B
  4. Chemotherapy
  5. Acyclovir
  6. Sulfonamides, cephalosporins
  7. Ethylene glycol
40
Q
  1. Contrast nephropathy is a form of what?
  2. Occurs how soon after exposure?
  3. Risk factors for development? 5
  4. Mechanism of injury unclear but likely involves? 5
A
  1. Form of ATN
  2. Occurs 24-48 h post contrast exposure
    • DM,
    • chronic kidney disease,
    • high contrast load,
    • concurrent use of nephrotoxic drugs,
    • age
    • direct toxicity of reactive oxygen species (free radicals)
    • contrast-induced diuresis
    • increased urinary viscosity
    • increased oxygen consumption
    • imbalance of vasoconstriction vs vasodilation
41
Q

Prevention of contrast nephropathy

5

A
  1. Minimize amount of contrast used…talk to radiologist
  2. Hydrate pre and post procedure with normal saline
  3. Mucomyst (N-Acetylcysteine) +/- (Also used for tylenol overdose)
  4. Stop metformin (glucophage) the day of contrast load and for 48 h post (can lead to lactic acidosis)
  5. Do you need this test? Alternatives?
42
Q

Further toxins
that could cause ATN?
4

A
  1. Blood transfusion reaction causing hemolytic anemia
  2. Multiple myeloma
  3. Uric acid
  4. Myoglobin
43
Q

Why would we get large amonts of myoglobin?

6

A
  1. Muscle breakdown, when severe called rhabdomyolysis (CK > 16,000)
  2. Crush injuries,
  3. muscle necrosis from pressure points in unconcious patients,
  4. seizures,
  5. cocaine,
  6. ETOH
44
Q

FENa (Fractional excretion of sodium and urine sodium concentration) is useful for what?

A

Useful for determining if the cause of acute kidney injury is prerenal or ATN

45
Q

If its prerenal FENa what will the level be at?

If its intrinsic FENa what will be the level?

A

Prerenal if FENa less than 1%

Intrinsic if FENa is > 2%

46
Q

What is the equation for FEna?

A

100 x (UNa x PCR)/(PNa x UCR)

47
Q 
Renal tubular cells inthe urine sediment.
Associated Urine particle:
1. Dark granular  and epithelial  casts?
2. Crystals?
3. WBCs and WBC casts?
4. RBCs and RBC casts?
A
  1. Pure ATN
  2. Crystalluric ARF
  3. Acute interstitial nephritis
  4. Proliferative/Nectrotizing glomerulonephritis
48
Q

Principals of management of acute kidney injury

6

A
  1. Treat underlying cause
  2. Maintain euvolemia
  3. Manage electrolytes
  4. Manage blood pressure
  5. Stop potentially nephrotoxic meds
  6. May need temporary dialysis
49
Q

Overview of the general work up

5

A
  1. Assess volume status
  2. Urinalysis
  3. CBC
  4. Serum BUN and Creatinine (BMP at a minimum)
  5. Fractional excretion of sodium
50
Q

What kind of urinalysis do we do for ARF?

4

A
  1. Dipstick,
  2. microscopic exam,
  3. urine sodium,
  4. urine creatinine
51
Q

Imaging studies
used for ARF?
4

A
  1. Renal ultrasound
  2. Bladder scan for post void residual
  3. CT or MRI
  4. Renal biopsy in certain cases
52
Q

State the levels for the following in Prerenal, Instristic, and Postrenal failure:

  1. Urina Na?
  2. BUN/Creat Ratio?
  3. FENa?
A

Prerenal

  1. less than 20
  2. > 20:1 (>20)
  3. less than 1

Intrinsic

  1. > 20
  2. less than 10:1 (less than 20)
  3. > 2

Postrenal

  1. variable
  2. 10-20:1 (less than 20)
  3. variable
53
Q
  1. Which one is the most common?

2. What test is the most important noninvasive test in the diagnostic evaluation of these patients?

A
  1. Intrinsic

2. UA

Nephrology (15 decks)

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