Oxalate occurs in many plants, where it is synthesized by the incomplete oxidation of carbohydrates.
Secondary hyperoxaluria is caused by increased oxalate absorption from the intestine or excessive dietary intake of oxalate such as with rhubarb, spinach, parsley, and cocoa or its precursor ascorbic acid.
Ascorbic acid increases the risk of plasma calcium oxalate supersaturation, particularly among patients undergoing hemodialysis.
Increased intestinal oxalate absorption in most commonly caused by fat malabsorption, as in inflammatory bowel disease patients who have undergone Roux-en-Y gastric bypass.
Normally oxalate binds preferentially to calcium in the gut, forming insoluble calcium salts that are excreted in the stool.
When there is malabsorption, excessive excess fatty acids complete for calcium binding, leaving increased levels of unbound oxalate to be absorbed in the intestine.
Oxalate-rich plants include fat hen sorrel, and several Oxalis species,the root and/or leaves of rhubarb and buckwheat, star fruit, black pepper, parsley, poppy seed, spinach, chard, beets, cocoa, chocolate, most nuts, most b2241ies, fishtail palms, New Zealand spinach and beans.
Leaves of the tea plant (Camellia sinensis) contain among the greatest measured concentrations of oxalic acid relative to other plants.
Common high-oxalate foods.
Food item Oxalate content mg.
Beetroot greens, cooked 1⁄2 cup 916 mg
Purslane, leaves, cooked 1⁄2 cup 910mg
Rhubarb, stewed, no sugar 1⁄2 cup 860 mg
Spinach, cooked 1⁄2 cup 750 mg
Beet, cooked 1⁄2 cup 675 mg
Chard, Swiss, leaves cooked 1⁄2 cup 660mg
Rhubarb, canned 1⁄2 cup 600mg
Spinach, frozen 1⁄2 cup 600mg
Beet, pickled 1⁄2 cup 500 mg
Poke greens, cooked 1⁄2 cup 476mg
Endive, raw 20 long leaves 273mg
Cocoa, dry 1⁄3 cup 254mg
Dandelion greens, cooked 1⁄2 cup 246mg
Okra, cooked 8–9 pods 146mg
Sweet potato, cooked 1⁄2 cup 141mg
Kale, cooked 1⁄2 cup 125mg
Peanuts, raw 1⁄3 cup (1 3⁄4 oz) 113mg
Turnip greens, cooked 1⁄2 cup 110mg
Chocolate, unsweetened 1 oz 91mg
Parsnips, diced, cooked 1⁄2 cup 81mg
Collard greens, cooked 1⁄2 cup 74mg
Pecans, halves, raw 1⁄3 cup (1 1⁄4 oz) 74mg
Tea, leaves (4-minute infusion) 1 level tsp in 7 fl oz water mg72
Cereal germ, toasted 1⁄4 cup 67mg
Gooseberries 1⁄2 cup 66mg
Potato, Idaho white, baked 1 medium 64mg
Carrots, cooked 1⁄2 cup 45mg
Apple, raw with skin 1 medium 41mg
Brussels sprouts, cooked 6–8 medium 37mg
Strawb2241ies, raw 1⁄2 cup 35mg
Celery, raw 2 stalks 34mg
Milk chocolate bar 1 bar (1.02 oz) 34mg
Raspberries, black, raw 1⁄2 cup 33mg
Orange, edible portion 1 medium 24mg
Green beans, cooked 1⁄2 cup 23mg
Chives, raw, chopped 1 tablespoon 19mg
Leeks, raw 1⁄2 medium 15mg
Blackberries, raw 1⁄2 cup 13mg
Concord grapes 1⁄2 cup 13mg
Blueberries, raw 1⁄2 cup 11mg
Redcurrants 1⁄2 cup 11mg
Apricots, raw 2 medium 10mg
Raspberries red, raw 1⁄2 cup 10mg
Broccoli, cooked 1 large stalk 6mg
Cranberry juice 1⁄2 cup (4 oz) 6mg
Recommendations in the dietary treatment of hypercalciuria:
Limit daily calcium intake to 600-800 mg/day.
Limit dietary oxalate, especially when calcium intake is reduced.
High oxalate levels are found in strong teas; nuts; chocolate; coffee; colas; green, leafy vegetables and other plant and vegetable products.
Oxalic acid combines with divalent metallic cations such as calcium (Ca2+) and iron(II) (Fe2+) to form crystals of the corresponding oxalates which are then excreted in urine as minute crystals.
Oxalates can form larger kidney stones that can obstruct the kidney tubules.
An estimated 80% of kidney stones are formed from calcium oxalate.
Those who should avoid food with high oxalate content include: patients with kidney disease, gout, rheumatoid arthritis, and vulvodynia.
Magnesium (Mg2+) oxalate is more than 500 times more soluble than calcium oxalate, so the latter is more likely to precipitate out when magnesium levels are low and calcium and oxalate levels are high.
Kidney damage is caused by oxalate crystals deposition in the renal tubular lumen.
The highly insoluble iron oxalate appears to play a major role in gout.
Foods high in oxalate should be avoided by people suffering from, or at risk of gout.
Evidence indicates the administration of probiotics can increase oxalic acid excretion.
Excess oxalate level in the blood is termed hyperoxalemia.
High levels of oxalate in the urine is termed hyperoxaluria.
Consumption of oxalates, such as excessive quantities of black tea may result in kidney disease or even death due to oxalate poisoning.
Oxalate nephropathy refers to kidney damage caused by oxalate crystals deposition in the renal tubular lumen.
Fat malabsorbed leads to increased free fatty acids in the intestine and competitive binding of fatty acids to calcium may result in increased intestinal oxalate absorption, increased renal oxalate excretion and the tendency to tubular calcium oxalate precipitation.
To confirm hyperoxaluria includes 24 hour urinary oxalate excretion, a random urinary oxalate level, urinary glycolate, glycerate, and hydroxy-1 oxoglutaraterate levels, plasma oxalate levels and genetic testing for primary hyperoxaluria.
Plasma oxalate levels in the normal range or 1-5 micro moles per liter, plasma oxalate levels are often higher than 80 µmol believer in patients with primary hyperoxaluria and between 20 and 80 µmol, in patients with secondary hyperoxaluria.