Balance studies and
oxalate loading tests were carried out in order to define the pathogenesis of
hyperoxaluria in 8 patients with
jejunoileal bypass surgery for
severe obesity; two healthy volunteers were also studied. In the bypass patients, urinary
oxalate was markedly elevated (118 +/- 43 mg/day, mean +/- SD) when they were on a high
oxalate diet (252 mg/day). Hyperabsorption of dietary
oxalate was confirmed by the markedly increased urinary recovery of [14C]
oxalate given in a test meal. In addition, the
oxalate radioactivity was excreted in urine far more slowly than in healthy volunteers, suggesting that the colon was a major site of
oxalate absorption. Elevated urinary
oxalate excretion persisted, averaging 38 +/- 12 mg/day, despite ingestion of a very low
oxalate diet (approximately 6 mg/day), suggesting that the diet contained "oxalogenic" substances other than preformed dietary
oxalate which also contributed to dietary
oxalate in these patients. Urinary
oxalate decreased in 7 of 8 patients, however, when
protein-rich foods were removed from the diet, suggesting that at least one dietary factor was digestive products of
protein or
creatinine. These results confirm the current view that in patients with
hyperoxaluria secondary to
jejunoileal bypass, the majority of urinary
oxalate derives from dietary
oxalate that is absorbed from the colon. Tissue or bacterial production of
oxalate or an
oxalate precursor from dietary constituents associated with
protein, however, also appears to contribute to urinary
oxalate. The results provide an explanation for the reported difficulty of eliminating secondary
hyperoxaluria by restriction of dietary
oxalate alone.