Urine Composition in Normal Subjects after Oral Ingestion of Oxalate-Rich Foods

Abstract

1. Urinary composition was studied in nine healthy adults on unrestricted diet and low-oxalate diet with and without individual oxalate-rich foods. 2. Urine oxalate was constant on the low-oxalate and constant high-oxalate diets and only fluctuated greatly on unrestricted diet. 3. Urine oxalate was mainly due to dietary oxalate which accounts for up to two-thirds of urinary oxalate. 4. Urine oxalate was unaffected by urine volume. 5. Varying percentages of dietary oxalate were absorbed depending on the nature of the foodstuff. 6. Although tea was the main source of dietary oxalate in some people it, like strawberries, did not represent a real risk factor. Chocolates, peanuts, beetroot, rhubarb and spinach were considered as high-risk foods. 7. Calcium oxalate crystalluria at 4 degrees C was increased significantly when the oxalate-rich foods were taken. When urine was examined at 37 degrees C no increase in crystalluria was found.

Bioavailability of soluble oxalate from tea and the effect of consuming milk with the tea

“…These values are comparable to previously determined availability of soluble oxalates from other foods for instance 2.4% (Brinkley et al, 1981) and oca 2.4% (Albihn & Savage, 2001b). In contrast, earlier reports on the availability of oxalate from lower intakes of oxalate from tea report an availability of 22.2% calculated from a 24 h collection on three subjects (Finch et al, 1981) while Brinkley et al (1990) determined the availability calculated over an 8 h period from a single ingestion of 1.4 g oxalate from tea to be 0.08%.…”

“…Consumption of tea without milk has been shown to increase urinary oxalate concentrations (Brinkley et al, 1990;Finch et al, 1981). These findings have prompted a recommendation to eliminate black tea from the diets of those people who form oxalate stones (Massey et al, 1993).…”

Management of patients with a short bowel

“…Under normal circumstances, most urinary oxalate derives from the metabolism of amino acids (mainly glycine) and of ascorbic acid. Less than 10% is derived from dietary oxalate [182] . However after an ileal resection there is increased colonic absorption of dietary oxalate especially by the distal colon [183] .…”

Reduction of Oxalate Levels in Tomato Fruit and Consequent Metabolic Remodeling Following Overexpression of a Fungal Oxalate Decarboxylase

“…When oxalate-rich food crops are consumed in large quantities, they can cause primary and secondary hyperoxaluria in humans, which results in impaired renal function, disturbances in Gly metabolism, and reduced blood coagulability (de Castro, 1988;Conyers et al, 1990). Thus, excess ingestion of oxalate results in a variety of kidney-related disorders (Hodgkinson, 1970;Anderson et al, 1971;Suvachittanont et al, 1973;Finch et al, 1981;Curhan, 1997), in addition to neurolathyrism and coronary disease (Singh and Saxena, 1972). The precipitation of oxalic acid as calcium oxalate leads to kidney stones and hypocalcemia (Williams and Wandzilak, 1989) due to poor intestinal absorption of calcium ions in the presence of oxalate (Heaney et al, 1988;Kelsay et al, 1988).…”