Used to work up nephrolithiasis
Ambient (preferred) - 7 days
Refrigerated - 7 days
Frozen - 14 days
< 7 years: not established
7 - 14 years: 13 - 38 mg/24 hours
Male: 7 - 44 mg/24 hours
Female: 4 - 31 mg/24 hours
Patients who form calcium oxalate kidney stones appear to absorb and excrete a higher portion of dietary oxalate in urine than do normals. Hyperoxaluria is not uncommon in subjects with malabsorption. Twenty-four hour urine collections for oxalate are indicated in patients with surgical loss of distal small intestine, especially those with Crohn's disease. The incidence of nephrolithiasis in patients who have inflammatory bowel disease is 2.6% to 10%. Hyperoxaluria is regularly present after jejunoileal bypass for morbid obesity; such patients may develop nephrolithiasis. Used to work up nephrolithiasis.
Oxaluria is characteristic of ethylene glycol intoxication. Oxalic acid excretion is increased with methoxyflurane. Serum calcium and urinary calcium excretion are also commonly needed; calcium oxalate renal stones are common. Hyperoxaluria may occur with high intake of animal protein, purines, gelatin, calcium, strawberries, pepper, rhubarb, beans, beets, spinach, tomatoes, chocolate, cocoa, and tea. Hyperoxaluria is described with pyridoxine deficiency. Urinary oxalate derives from the metabolism of glycine and ascorbic acid more than from dietary ingestion. Oxalate excretion is increased in vegetarians, despite low animal protein ingestion. Vitamin C increases oxalate excretion and may be a riskfactor for calcium oxalate nephrolithiasis in individuals consuming "megadose" vitamin C. Such ingestion can usually be determined by the history. If a vitamin C using stone former is found to have high urine oxalate excretion, the habit should be stopped. If oxalate excretion drops to normal, additional therapy to prevent stones may not be required. Hyperoxaluria can result from intestinal hyperabsorption related to low calcium intake or high calcium enteric binding. Unabsorbed fat can bind calcium. Increased urinary uric acid excretion is frequently found in subjects who have calcium oxalate nephrolithiasis. Calcium nephrolithiasis in patients with hyperuricosuria has beenrelated to urate-induced crystallization of calcium oxalate. Urinary oxalate concentrations have been found to be increased in very low birth weight infants receiving parenteral amino acid solutions. Rare genetic disorders increase endogenous oxalate production; there are two types of primary hyperoxaluria. They are characterized by elevated urinary oxalate excretion and recurrent oxalate nephrocalcinosis. In type I, a defect in glyoxalate metabolism is found, leading to increased oxalate synthesis. Excessive quantities of glyoxylic and glycolic acid urinary excretion occur. Type II is rare; it is characterized by excessive urinary excretion of oxalic and L-glyceric acids with normalexcretion of glycolic acid.