Acute Tubular Necrosis Flashcards
What is acute tubular necrosis (ATN)?
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.
What is the most common intrinsic AKI?
Acute tubular necrosis (ATN).
How long does recovery from ATN take?
The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.
Give examples of causes of ATN
Note: hypoperfusion
Ischaemia can occur secondary to hypoperfusion in:
- Shock
- Sepsis
- Dehydration
Give examples of causes of ATN
Note: toxins
Direct damage from toxins can occur due to:
- Radiology contrast dye
- Gentamycin
- NSAIDs
What are the risk factors for ATN?
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
What are the signs of ATN?
- Hypotension
- Tachycardia
What are the symptoms of ATN?
- Oliguria or anuria
- Poor oral intake or anorexia
- Malaise
What investigations should be ordered for ATN?
- Basic metabolic profile
- Urea-to-creatinine ratio
- Urine sodium concentration
- Urine osmolarity
- Urinanalysis
- FBC
- Coagulation studies
- Urinary myoglobin
- ABG
Why investigate basic metabolic profile?
Note: urea and creatinine
Elevated serum creatinine, elevated urea, hyperkalaemia or metabolic acidosis suggests ATN.
Why investigate urea-to-creatinine ratio?
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.
Why investigate urine sodium concentration?
Tubule dysfunction leads to increased urinary sodium concentration.
Why investigate urine osmolarity?
Impairment in urinary concentrating capacity is characterised by decrease in urine osmolality. <450 mOsmol/kg supports ATN.
Why investigate urinanlysis for sediment?
Tubular epithelial cells, epithelial cell casts or muddy brown casts supports ATN.
Why investiate FBC?
Mild to moderate anaemia is commonly observed in some types of ATN, such as in multiple myeloma, bleeding, haemolysis, or chronic kidney disease.
Why investigate coagulation studies?
Prolonged ATN can result in bleeding as a result of dysfunctional platelets.
Why investigate urinary myoglobin?
Elevated myoglobin levels suggest ATN from rhabdomyolysis.
Why investigate using ABG?
Assists in further evaluation of acidosis, which is often suggested by the low bicarbonate on the basic metabolic profile.
May show metabolic acidosis.
What is the most “pathogenomic” finding of ATN on urinanlysis?
“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.
Briefly describe the management of ATN
Treatment is the same as with other causes of an acute kidney injury:
- Supportive management
- IV fluids
- Stop nephrotoxic medications
- Treat complications
When may renal replacement therapy be considered in ATN?
Severe acidosis, volume overload refractory to diuretics, hyperkalaemia or uraemia.
What are the complications of ATN?
- Anaemia
- Hyperkalaemia
- Metabolic acidosis
- End stage renal disease
- Uraemia
What differentials should be considered for ATN?
- Pre-renal azotaemia
- Intrinsic azotaemia
How does ATN and pre-renal azotaemia differ?
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
How does ATN and instrinsic renal azotaemia differ?
Differentiating signs and symptoms:
- Patients with glomerular disease typically present with proteinuria and microscopic dysmorphic haematuria
Differentiating investigations:
- Urinalysis shows proteinuria and microscopic haematuria