Miscellaneous

Question 1

How does RAAS prevent ischaemia and maintain blood flow?

Answer 1

• Increases circulating volume by increasing Na+ reabsorption and water
• Vasoconstricts the efferent renal arteriole to maintain GFR
  Local protection of the nephron

Question 2

How do ACE-i, ARBs and NSAIDs damage the kidneys?

Answer 2

Make the protective RAAS mechanism less likely

- Makes tubular ischaemia and necrosis more likely

Question 3

What is acute tubular necrosis (ATN)?

Answer 3

It is an intrinsic AKI that follows a condition of severe and persistent hypoperfusion or toxic injury of epithelial cells causing detachment from the basement membrane and tubular dysfunction.

Question 4

What does the histology show for acute tubular necrosis (ATN)?

Answer 4

• Tubular epithelium necrosis
• Sloughing of the renal tubular epithelium causing dilation and obstruction of tubules
• Mild leucocyte infiltration

Question 5

How do you treat acute tubular necrosis (ATN)?

Answer 5

• Supportive
• Withdrawal of nephrotoxic agents
• Treatment of associated sepsis

Question 6

What is the prognosis of acute tubular necrosis (ATN)?

Answer 6

• Usually, recovery after 2-3 weeks

- High mortality associated with ATN, usually due to the associated illness (septic shock), age etc.

Question 7

What is the oligouric phase of acute tubular necrosis (ATN)?

Answer 7

• <500mls urine production in one day
• Patients are vulnerable to fluid overload and electrolyte imbalances
• Creatinine levels rise rapidly

Question 8

What is the maintenance phase of acute tubular necrosis (ATN)?

Answer 8

• Increases urinary output helps to maintain fluid and electrolyte balance
• Creatinine levels are stable or rise slowly

Question 9

What is the polyuric recovery phase of acute tubular necrosis (ATN)?

Answer 9

• Kidneys produce large amounts of dilute urine -> patients become hypovolaemic and unwell
• Creatinine levels fall swiftly