Urine Oxalate

General Information

Oxalate in urine may arise either as an end-product of the metabolism of ascorbic acid and amino acids (especially glycine) or from dietary sources (e.g. rhubarb, spinach, tea). Hyperoxaluria leads to the formation of highly insoluble calcium oxalate which has a tendency to precipitate out in the renal medulla and urine leading to urolithiasis.

There are two forms of primary hyperoxaluria. Type I hyperoxaluria is associated with an increase in urine glycolate caused by deficiency of the peroxisomal enzyme alanine : glyoxylate aminotransferase (AGT). Patients present in the first decade of life with recurrent calcium oxalate nephrolithiasis. Type II hyperoxaluria is associated with an increase in urine L-glyceric acid caused by deficiency of the cytosolic enzyme D-glycerate dehydrogenase. Survival of these patients appears to be better than those with type I hyperoxaluria.

Hyperoxaluria may also occur secondary to inflammatory bowel disease or malabsorption. This may be due to a reduction in the levels of calcium in the gut, as the ionised calcium ion concentration is a limiting factor in oxalate absorption and low levels promote oxalate absorption.