BACKGROUND: Hyperoxaluria and increased calcium oxalate stone formation occur 
after Roux-en-Y gastric bypass (RYGB) surgery for morbid obesity. The etiology 
of this hyperoxaluria is unknown. We hypothesized that after bariatric surgery, 
intestinal hyperabsorption of oxalate contributes to increases in plasma oxalate 
and urinary calcium oxalate supersaturation.
METHODS: We prospectively examined oxalate metabolism in 11 morbidly obese 
subjects before and 6 and 12 months after RYGB (n = 9) and biliopancreatic 
diversion-duodenal switch (BPD-DS) (n = 2). We measured 24-hour urinary 
supersaturations for calcium oxalate, apatite, brushite, uric acid, and sodium 
urate; fasting plasma oxalate; 72-hour fecal fat; and increases in urine oxalate 
following an oral oxalate load.
RESULTS: Six and 12 months after RYGB, plasma oxalate and urine calcium oxalate 
supersaturation increased significantly compared with similar measurements 
obtained before surgery (all P ≤ .02). Fecal fat excretion at 6 and 12 months 
was increased (P = .026 and .055, 0 vs 6 and 12 months). An increase in urine 
oxalate excretion after an oral dose of oxalate was observed at 6 and 12 months 
(all P ≤ .02). Therefore, after bariatric surgery, increases in fecal fat 
excretion, urinary oxalate excretion after an oral oxalate load, plasma oxalate, 
and urinary calcium oxalate supersaturation values were observed.
CONCLUSION: Enteric hyperoxaluria is often present in patients after the 
operations of RYGB and BPD-DS that utilize an element of intestinal 
malabsorption as a mechanism for weight loss.