Intestinal absorption of oxalate was assessed indirectly from the increase in renal oxalate excretion following the oral administration of 5 mmol of stable oxalate. When sodium oxalate alone was given without divalent cations to patients in the fasting state, the urinary oxalate increased promptly (within 2 hours). The increase was more prominent and sustained in those with ileal disease (ileal resection or jujunoileal bypass); thus, 35 per cent of the orally administered oxalate eventually appeared in the urine in the group with ileal disease, 8 per cent in the group with stones (renal and absorptive hypercalciurias) and 9 per cent in the control group. This hyperexcretion of oxalate could be largely, but not totally, ameliorated by the concurrent oral administration of divalent cations. Although urinary oxalate decreased significantly following the oral administration of calcium or magnesium, hyperoxaluria persisted in most patients. The results suggested that the hyperabsorption of oxalate in ileal disease cannot be accounted for solely by an increased absorbable oxalate pool associated with calcium-fatty acid complexation. Moreover, although urinary oxalate decreased, urinary calcium increased concurrently when either calcium or magnesium was given. Thus, there was no significant change or increase in the urinary state of saturation with respect to calcium oxalate.
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