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Y3 Medicine: Renal > Acute Tubular Necrosis > Flashcards

Acute Tubular Necrosis Flashcards

1
Q

What is acute tubular necrosis (ATN)?

A

Acute tubular necrosis (ATN) is an intrinsic AKI that follows a condition of severe and persistent hypoperfusion or toxic injury of epithelial cells causing detachment of the basement membrane and tubular dysfunction.

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2
Q

What is the most common intrinsic AKI?

A

Acute tubular necrosis (ATN).

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3
Q

How long does recovery from ATN take?

A

The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.

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4
Q

Give examples of causes of ATN

Note: hypoperfusion

A

Ischaemia can occur secondary to hypoperfusion in:

  • Shock
  • Sepsis
  • Dehydration
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5
Q

Give examples of causes of ATN

Note: toxins

A

Direct damage from toxins can occur due to:

  • Radiology contrast dye
  • Gentamycin
  • NSAIDs
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6
Q

What are the risk factors for ATN?

A

Key risk factors include:

  • Low renal perfusion
  • Underlying renal disease
  • Diabetes mellitus
  • Hypotension
  • Multiple myeloma
  • Exposure to nephrotoxins or radiocontrast media
  • Excessive fluid loss
  • Sepsis
  • Major surgery
  • Cardiac arrest
  • Advanced age
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7
Q

What are the signs of ATN?

A
  • Hypotension
  • Tachycardia
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8
Q

What are the symptoms of ATN?

A
  • Oliguria or anuria
  • Poor oral intake or anorexia
  • Malaise
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9
Q

What investigations should be ordered for ATN?

A
  • Basic metabolic profile
  • Urea-to-creatinine ratio
  • Urine sodium concentration
  • Urine osmolarity
  • Urinanalysis
  • FBC
  • Coagulation studies
  • Urinary myoglobin
  • ABG
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10
Q

Why investigate basic metabolic profile?

Note: urea and creatinine

A

Elevated serum creatinine, elevated urea, hyperkalaemia or metabolic acidosis suggests ATN.

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11
Q

Why investigate urea-to-creatinine ratio?

A

In cases of ATN the ratio of blood urea to creatinine falls to 10:1, as tubular injury means there is no increased reabsorption of water, sodium, and urea.

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12
Q

Why investigate urine sodium concentration?

A

Tubule dysfunction leads to increased urinary sodium concentration.

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13
Q

Why investigate urine osmolarity?

A

Impairment in urinary concentrating capacity is characterised by decrease in urine osmolality. <450 mOsmol/kg supports ATN.

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14
Q

Why investigate urinanlysis for sediment?

A

Tubular epithelial cells, epithelial cell casts or muddy brown casts supports ATN.

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15
Q

Why investiate FBC?

A

Mild to moderate anaemia is commonly observed in some types of ATN, such as in multiple myeloma, bleeding, haemolysis, or chronic kidney disease.

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16
Q

Why investigate coagulation studies?

A

Prolonged ATN can result in bleeding as a result of dysfunctional platelets.

17
Q

Why investigate urinary myoglobin?

A

Elevated myoglobin levels suggest ATN from rhabdomyolysis.

18
Q

Why investigate using ABG?

A

Assists in further evaluation of acidosis, which is often suggested by the low bicarbonate on the basic metabolic profile.

May show metabolic acidosis.

19
Q

What is the most “pathogenomic” finding of ATN on urinanlysis?

A

“Muddy brown casts” found on urinalysis is a pathognomonic finding specific to acute tubular necrosis. There can also be renal tubular epithelial cells in the urine.

20
Q

Briefly describe the management of ATN

A

Treatment is the same as with other causes of an acute kidney injury:

  • Supportive management
  • IV fluids
  • Stop nephrotoxic medications
  • Treat complications
21
Q

When may renal replacement therapy be considered in ATN?

A

Severe acidosis, volume overload refractory to diuretics, hyperkalaemia or uraemia.

22
Q

What are the complications of ATN?

A
  • Anaemia
  • Hyperkalaemia
  • Metabolic acidosis
  • End stage renal disease
  • Uraemia
23
Q

What differentials should be considered for ATN?

A
  1. Pre-renal azotaemia
  2. Intrinsic azotaemia
24
Q

How does ATN and pre-renal azotaemia differ?

A

Differentiating signs and symptoms:

  • Oliguria is much more frequent

Differentiating investigations:

  • Urea-to-creatinine ratio is >20:1
  • Ratio of urine to plasma creatinine levels are high and the urinary sodium concentration is low
25
Q

How does ATN and instrinsic renal azotaemia differ?

A

Differentiating signs and symptoms:

  • Patients with glomerular disease typically present with proteinuria and microscopic dysmorphic haematuria

Differentiating investigations:

  • Urinalysis shows proteinuria and microscopic haematuria

Y3 Medicine: Renal (13 decks)

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