11.1 Acute Tubular Necrosis

Question 1

What is the most common cause of AKI?

Answer 1

Acute tubular necrosis (almost half)

Question 2

List two causes of pre, renal, post-renal AKI

Answer 2

• Pre (hypoperfusion): hypovolamiea, renal artery stenosis
• Renal (kidney dysfunction): nephrotoxic drugs, acute tubular necrosis
• Post (lower urinary tract): VUR, ureteric calculi

Question 3

List, with examples, three causes of Acute Tubular Necrosis

Answer 3

• Ischaemia
• Drugs (aminoglycoside, NSAIDs)
• Toxins (snake venom, heavy metals, myoglobin)

Question 4

List three risk factors for acute tubular necrosis

Answer 4

• Pre-existing renal disease
• Ageing
• Medications such as aminoglycosides and NSAIDs

Question 5

Describe the distribution of oxygen throughout the layers of the kidney. How does this affect the nephrons that are damaged first during renal ischaemia, and how might this affect urine?

Answer 5

• Cortex receives more blood, medulla gets less
• Therefore, juxtamedullary neurons die first
• These are responsible for urine concentration, so death of these may lead to weaker urine concentration

Question 6

List drug classes that can cause non-ischaemic ATN

Answer 6

• Anti-fungals
• Antibiotics (aminoglycosides, vanc)
• Antivirals
• Radiocontrast agents
• Platinum-based chemo (like a platinum card at an ATM)

Question 7

List toxins that can cause ATN

Answer 7

• Myoglobin
• Heavy metals
• Haemoglobin

Question 8

Describe the histopathological changes seen in ATN

Answer 8

• Flattened epitelium
• Loss of brush border
• Luminal obstruction with apoptotic/mitotic epithelial cells

Question 9

Typical Hx of pre-renal AKi vs ATN

Answer 9

Pre-renal: volume loss (burns, haemorrhage, heart failure)
ATN: prolonged haemodynamic compromise (?drugs/toxins)

Note: ATN is a type of AKI

Question 10

Urine protein in Pre-renal AKI vs ATN

Answer 10

• Pre-renal: low
• ATN: Higher

Question 11

Urine sodium in pre-renal AKI vs ATN

Answer 11

• Pre-renal: low (no blood reaches)
• ATN: higher (blood reaches; no resorption)

Question 12

What kind of casts are seen in ATN?

Answer 12

“Muddy brown” casts

Question 13

Is urea excretion higher in pre-renal AKi or ATN? Why?

Answer 13

• Higher in ATN
• More blood reaches nephron; even if reabsorptive capacity is lost, urea can still be excreted

Question 14

Clinical features of ATN

Answer 14

• Oliguria
• “Muddy brown” casts on urine microscopy
• Nausea/vomiting (?acidosis)
• Oedema (peripheral/pulmonary)

Question 15

ATN treatment

Answer 15

• SUPPORTIVE
• Reduce fluid intake/diuretics to help with oedema
• Dialysis if kidneys are really struggling

Question 16

Which responds faster to removal of the underlying cause, and why: pre-renal AKI, or ATN?

Answer 16

• Pre-renal responds faster
• Once kidneys are reperfused, this will return to normal (if completely pre-renal)
• In ATN, there is irreversible loss of nephrons, this does not recover as quickly

Question 17

Why is the fractional excretion of sodium higher in acute tubular necrosis than in pre-renal AKI?

Answer 17

• In pre-renal the nephrons are working. They detect low sodium, activating the RAAS system to decrease sodium loss.
• In ATN, the tubules aren’t working normally. They lose the ability to reabsorb sodium, meaning more stays in the urine, and the RAAS system is not functioning optimally either. Therefore, more sodium is lost, and the frac. excretion is lower.