|Values are valid only on day of printing.|
Oxalate is an end product of glyoxalate and glycerate metabolism. Humans have no enzyme capable of degrading oxalate, so it must be eliminated by the kidney.
In tubular fluid, oxalate can combine with calcium to form calcium oxalate stones. In addition, high concentrations of oxalate may be toxic for renal cells.
Increased urinary oxalate excretion results from inherited enzyme deficiencies (primary hyperoxaluria), gastrointestinal disorders associated with fat malabsorption (secondary hyperoxaluria), or increased oral intake of oxalate-rich foods or vitamin C.
Since increased urinary oxalate excretion promotes calcium oxalate stone formation, various strategies are employed to lower oxalate excretion.
Monitoring therapy for kidney stones
Identifying increased urinary oxalate as a risk factor for stone formation
Diagnosis of primary or secondary hyperoxaluria
An elevated urine oxalate (>0.46 mmol/day) may suggest disease states such as secondary hyperoxaluria (fat malabsorption), primary hyperoxaluria (alanine glyoxalate transferase enzyme deficiency, glyceric dehydrogenase deficiency), idiopathic hyperoxaluria, or excess dietary oxalate or vitamin C intake.
In stone-forming patients high urinary oxalate values, sometimes even in the upper limit of the normal range, are treated to reduce the risk of stone formation.
Ingestion of ascorbic acid (>2 g/day) may falsely elevate the measured urinary oxalate excretion.
Do not collect in metal-capped containers.
The reference value is for a 24-hour collection. Specimens collected for other than a 24-hour time period are reported in unit of mmol/L for which reference values are not established.
Wilson DM, Liedtke RR: Modified enzyme-based colorimetric assay of urinary and plasma oxalate with improved sensitivity and no ascorbate interference: reference values and sample handling procedures. Clin Chem 1991;37:1229-1235