IVIg Sucrose Osmotic Nephrosis Proximal Tubule — ESENeph MCQ

Instant feedback + full explanation. One question, done properly.

HardAcute Kidney InjuryIVIg Sucrose Osmotic Nephrosis Proximal TubuleESENeph

A 38-year-old man develops AKI after receiving high-dose IV immunoglobulin (IVIg) for Guillain-Barré syndrome. His creatinine rises from 85 to 320 umol/L over 4 days. Urine microscopy is bland. Renal biopsy shows isometric vacuolisation of proximal tubular epithelial cells with PAS-positive droplets. What is the mechanism of AKI?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: B — Osmotic nephrosis from sucrose-stabilised IVIg

IVIg-associated AKI is caused by osmotic nephrosis, specifically from the sucrose stabiliser used in some IVIg formulations. Sucrose is taken up by proximal tubular cells via pinocytosis but cannot be metabolised, causing osmotic swelling and vacuolisation — 'osmotic nephrosis.' The characteristic biopsy finding is isometric cytoplasmic vacuolisation of proximal tubular cells with PAS-positive inclusions. Risk factors include CKD, volume depletion, diabetes, and high infusion rate. AKI is usually reversible but can be severe. Prevention involves using sucrose-free IVIg preparations, ensuring adequate hydration, and slowing infusion rates. Modern IVIg products increasingly use alternative stabilisers (L-proline, glycine) to avoid this complication.

Reference: Levy & Bhatt 2005 – IVIg Osmotic Nephrosis; JRCPTB 2022 – Nephrology Curriculum