Abstract

The hyperoxaluria frequently observed in patients with ileal dysfunction has been attributed to increased intestinal absorption of dietary oxalate. Studies of intestinal oxalate transport were performed to provide understanding of this augmentation of oxalate absorption. Uptake of oxalate by rabbit ileum did not result in mucosal accumulation. Increasing oxalate concentrations were associated with increased rates of uptake, and metabolic inhibitors did not alter uptake. Oxalate transport across everted rat duodenum, jejunum, ileum, and colon did not demonstrate active transport. These studies suggest that oxalate transport is a nonenergy-dependent, nonsaturable process. In additional experiments, alterations of oxalate solubility were produced in vitro by cholestyramine, calcium chloride, and sodium oleate. Since the rate of oxalate absorption will be determined by the oxalate concentration, changes in oxalate solubility may, in part, explain the increased oxalate absorption of ileal disease.

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