Enteric Hyperoxaluria

Nephrolithiasismedium

A 49-year-old man with obesity, hypertension, and gout undergoes Roux-en-Y gastric bypass. His medications include lisinopril, furosemide, ibuprofen, and glyburide. About 4-5 weeks later he presents with weakness and fatigue; serum creatinine has risen to 3.7 mg/dL from a normal baseline. Urine microscopy shows 1-3 RBCs/hpf, occasional renal tubular epithelial cells, and abundant colorless, bipyramidal (envelope-shaped) crystals; a kidney biopsy shows tubular crystal deposition that is birefringent under polarized light. Which of the following crystals is MOST likely responsible?

  1. A.Calcium phosphate crystals
  2. B.Uric acid crystals
  3. C.Cystine crystals
  4. D.Calcium oxalate crystalsCorrect

Explanation

This is acute oxalate nephropathy from enteric hyperoxaluria after Roux-en-Y gastric bypass. Fat malabsorption leaves free fatty acids in the gut lumen that saponify calcium; unbound oxalate is then absorbed, producing hyperoxaluria and tubular calcium-oxalate deposition and AKI. Calcium-oxalate dihydrate crystals are the colorless, bipyramidal (envelope) forms described and are birefringent. The other crystals do not fit the malabsorptive post-bypass setting or the morphology.

Why each option

A.
Calcium phosphate crystals occur with alkaline urine/distal RTA, not enteric hyperoxaluria after bypass.
B.
Uric acid crystals form in acidic urine and are unrelated to fat-malabsorptive oxalate nephropathy.
C.
Cystine crystals are hexagonal and occur only in the genetic disorder cystinuria.
D.
Correct. Envelope-shaped calcium-oxalate crystals reflect enteric hyperoxaluria and oxalate nephropathy after Roux-en-Y bypass.

Reference: Nasr SH et al. Oxalate nephropathy complicating Roux-en-Y gastric bypass. Clin J Am Soc Nephrol 2008;3:1676-1683.

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