MBBS viva
Contrast-Associated AKI & Acute Tubular Necrosis vs Pre-Renal AKI — Viva
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Q1: Definition and the pre-renal vs ATN distinction (3 min)
Define contrast-associated AKI and state the ESUR/ACR criteria precisely (0.3 mg/dL rise or 1.5x baseline within 48-72 h of iodinated contrast).
How would you distinguish pre-renal azotaemia from acute tubular necrosis at the bedside? Reproduce the urine sodium, FENa, urine osmolality, BUN/creatinine ratio and urine sediment findings for each. State the formula for FENa and its limitations (diuretics - use FEurea under 35 percent; sepsis; bicarbonaturia; chronic CKD).
Why is pre-renal AKI rapidly reversible while ATN takes days to weeks to recover?
Q2: Pathophysiology (3 min)
Explain the two mechanisms by which iodinated contrast causes acute tubular necrosis - renal medullary vasoconstriction and direct tubular cytotoxicity. Which nephron segments are most vulnerable (S3 proximal tubule and medullary thick ascending limb) and why (operate on the brink of hypoxia)?
List the four mechanisms by which ischaemic or nephrotoxic injury lowers GFR in ATN - tubular cell injury and death, cast obstruction, back-leak of filtrate, and afferent arteriolar vasoconstriction.
Describe pigment nephropathy from rhabdomyolysis - how myoglobin causes cast formation, lipid peroxidation (ferrous iron, Fenton chemistry) and nitric oxide consumption. What is the dipstick clue (positive for blood, no red cells on microscopy)?
Q3: Prevention and management (3 min)
State the four pillars of contrast-associated AKI prevention. What is the single best-proven measure? Reproduce the KDIGO hydration protocol for elective and urgent settings.
What did the PRESERVE trial (Weisbord, NEJM 2018) show about N-acetylcysteine and sodium bicarbonate? What did the AMACING trial (Lancet 2017) show about routine prophylactic hydration in moderate-risk patients?
Reproduce the metformin-and-contrast rule. Why is metformin held?
Q4: Severe AKI and renal replacement therapy (2 min)
Reproduce the AEIOU indications for renal replacement therapy. When would you call nephrology and ICU?
State the findings of the AKIKI (NEJM 2016) and STARRT-AKI (NEJM 2020) trials on the timing of RRT in critically ill AKI - what is the current practice?
Reproduce the hyperkalaemia treatment ladder with doses (calcium gluconate 10% 10 mL; insulin 10 units with 25 g dextrose; salbutamol 10-20 mg neb; sodium polystyrene sulfonate 15-30 g; dialysis).
Q5: Pitfalls and differentials (2 min)
How would you distinguish contrast-associated AKI from cholesterol atheroembolisation after a catheter procedure (timing, livedo, blue toes, eosinophilia, complement)?
What is the polyuric phase of ATN recovery, and what are its risks?
Why are FENa and urine sodium unreliable after diuretics? Which index do you use instead?