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Enteric Hyperoxaluria Post-Bariatric Mechanism — ESENeph MCQ

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ModerateRenal Stone DiseaseEnteric Hyperoxaluria Post-Bariatric MechanismESENeph

A 38-year-old woman has recurrent calcium oxalate nephrolithiasis. She undergoes metabolic evaluation. 24-hour urine: calcium 3.2 mmol/day (normal), oxalate 1.1 mmol/day (elevated), citrate 2.5 mmol/day (normal), urine volume 2.5 L. She takes no supplements. She has had bariatric surgery (Roux-en-Y gastric bypass) 3 years ago. What is the mechanism of her hyperoxaluria?

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Correct answer: E — Enteric hyperoxaluria from fat malabsorption

Roux-en-Y gastric bypass causes enteric hyperoxaluria through fat malabsorption. Unabsorbed fatty acids in the gut bind calcium (forming insoluble calcium soaps), leaving free oxalate unbound and available for absorption in the colon. Normally, dietary calcium binds oxalate in the gut lumen, preventing its absorption. Post-bariatric surgery, this protective calcium-oxalate binding is disrupted. Additionally, bile salt malabsorption increases colonic permeability to oxalate. Management includes: oral calcium supplements WITH meals (to bind oxalate in the gut), adequate hydration, potassium citrate, and dietary oxalate restriction. This is a growing clinical problem with increasing bariatric surgery rates.

Reference: https://guidelines.ukkidney.org