Calcium oxalate absorption

Calcium oxalate (723) occurs as the monohydrate (whewellite, the thermodynamically stable form under ambient conditions (724)), the dihydrate (weddellite) in plant calcium stores and in sap, or the trihydrate (725). Calcium oxalate also plays a structural role in plants. Oxalate, for example from excessive amounts of rhubarb or spinach, inhibits absorption of Ca2+ from the GIT precipitation of calcium oxalate is the reason for the toxicity of oxalates. Calcium oxalate may also occur in man, where it can appear as minute star-shaped crystals in the urine. It is the main constituent of the majority of urinary calculi in man (726,727). The relationships between dietary calcium... 

Of nutrient chelates in the human diet, oxalates and phytules arc Ihe most common. Oxalic acid, found principally in spinach, rhubarb leaves, beet leaves, some fruits, and mushrooms, is u primary chelator of calcium. Oxalate present in pineapple, kiwifmil, and possibly in other foods, occurs as calcium oxalale. CaCiOj. This compound is in the form of needle-like crystals, known as raphidcs. which can produce painful sensations in the mouth when eaten raw. The effects of oxalic acid in the diet may he twofold. First, it forms strong chelates with dietary calcium, rendering the culcium unavailable for absorption and assimilation. Secondly, absorbed oxalic acid causes assimilated Ca to be precipitated as insoluble salts that accumulate in the renal glomeruli and contribute to the formation of renal calculi. 

Approximately two thirds of all renal stones contain calcium phosphate or calcium oxalate. Many patients with such stones exhibit a renal defect in calcium reabsorption that causes hypercalciuria. This can be treated with thiazide diuretics, which enhance calcium reabsorption in the distal convoluted tubule and thus reduce the urinary calcium concentration. Salt intake must be reduced in this setting, as excess dietary NaCl will overwhelm the hypocalciuric effect of thiazides. Calcium stones may also be caused by increased intestinal absorption of calcium, or they may be idiopathic. In these situations, thiazides are also effective, but should be used as adjunctive therapy with decreased calcium intake and other measures. 

Dietary oxalate is absorbed throughout the length of the intestine, but mainly in the small intestine [3]. Oxalate absorption from the gut is dependent on the amount of free oxalate present in the intestinal lumen, often referred to as bioavailable oxalate. When calcium is plentiful in the gut, a greater proportion of oxalate will be complexed to the cations leaving less free for absorption. Hence patients with hyperoxaluria should be advised to consume a calcium rich diet. 

In a recent publication Sikora et al. found that increased intestinal oxalate absorption is an important risk factor for idiopathic calcium oxalate nephrolithiasis [16]. This observation may have important implications for the prevention of this disease. 

Sikora P, von Unruh G, Beck B, Eeldkotter M, Zajaczdowska M, Hesse A et al. [13C2] Oxalate absorption in children with idiopathic calcium oxalate urolithiasis or primary hyperoxaluria. Kidney Int. 2008 73 1181-6. 

However, convincing evidence questions the usefulness of this classification and these therapeutic approaches. Dietary restriction of calcium is now generally regarded as ineffective, and actually counterproductive, as it results in an increase in intestinal oxalate absorption and increased risk of stone formation. Further, patients with hypercalciuria are known to have reduced bone mineral density, and dietary calcium restriction may exacerbate a tendency to osteopenia and/or osteoporosis. ... 

With calcium stone disease, magnesium is an inhibitor of stone growth. Magnesium forms complexes with oxalate that are more soluble than calcium oxalate. Increased urinary magnesium therefore inhibits stone formation. Administration of magnesium has been shown to reduce enteral calcium absorption and has been proposed as a treatment for idiopathic hypercalciuric stone formers. However, oral magnesium supplementation may have unpleasant side effects and a positive benefit in terms of reducing stone recurrence has not been demonstrated. ... 

Oxalate is an end product of metabolism, predominantly derived from breakdown of glyoxylate and glycine. Plasma concentration of oxalate is 1,0 to 2.4mg/L (11 to 27fxmol/L) and it is excreted in the urine at a rate of 17.5 to 35.1 mg/24 hours (200 to 400pmol/24 hours). Only 10% to 15% of urinary oxalate is derived directly from dietary sources. Intestinal oxalate absorption is increased when the availability of calcium in the intestine is reduced. Hyperoxaluria is... 

For example, we showed in earlier chapters that the calcium ion concentration of an aqueous solution is readily determined by titration with a standard EDTA solution or by potential measurements with a specific-ion electrode. Alternatively, the calcium content of a solution can be determined either from atomic absorption or atomic emission measurements or by the precipitation of calcium oxalate followed by weighing or titrating with a standard solution of potassium permanganate. 

As intestinal absorption of calcium increases, urinary calcium excretion also increases. When the latter exceeds 300 mg/d, formation of calcium phosphate or calcium oxalate stones (urolithiasis) may occur. Hypercalciuria may result from decreased reabsorption of calcium due to a renal tubular defect or from increased intestinal absorption of calcium. Hypercalciuria may be due to an intrinsic defect in the intestinal mucosa or secondary to increased synthesis of 1,25-(OH)2D in the kidney. Disordered regulation of 1,25-(0H)2D synthesis is relatively common in idiopathic hypercalciuria. Treatment usually includes reduction in dietary calcium. Increased vitamin D intake, hyperparathyroidism, and other disorders can also cause hypercalciuria and urolithiasis. 

In some forms of steatorrhea, calcium, which normally binds to and precipitates oxalate in the intestine, binds instead to fatty acids producing increased oxalate absorption and hyperoxaluria. Even though urinary calcium is decreased under these conditions, the concentration of urinary oxalate may be elevated sufficiently to cause precipitation of calcium oxalate crystals. Stone formation can be exacerbated by a diet that contains foods rich in oxalate, such as rhubarb, citrus fruits, tea, and cola drinks. 

Increased oxalate absorption can be reduced by calcium administered with meals as a water-soluble salt. 

Systemic complications of Crohn s disease are common, and similar to those found with ulcerative colitis. Arthritis, iritis, skin lesions, and liver disease often accompany Crohn s disease. Renal stones occur in up to 10% of patients with Crohn s disease (less frequently with ulcerative colitis) and are caused by fat malabsorption, which allows for greater oxalate absorption and formation of calcium oxalate stones. Gallstones also occur with greater frequency in patients with ileitis, possibly because of bile acid malabsorption at the terminal ileum. 

The only common redox titration applied in the clinical laboratory is for the analysis of calcium in biological fluids. Calcium oxalate is precipitated and filtered, the precipitate is dissolved in acid, and the oxalate, which is equivalent to the calcium present, is titrated with standard potassium permanganate solution. This method is largely replaced now by more convenient techniques such as complex-ometric titration with EDTA (Chapter 9) or measurement by atomic absorption spectrophotometry (Chapter 17). 

Recently, the determination of calcium and magnesium by atomic absorption spectrometry is preferred gravimetric and manganometric determinations after elimination of calcium in the form of calcium oxalate are losing their importance [14]. 

Sodium cellulose phosphate (SCP) is an insoluble, non-absorbable ester of cellulose containing 34% inorganic phosphate and 11% sodium. It is capable of binding calcium in the intestinal tract, reducing absorption of this ion, as well as magnesium. SCP is indicated only for the treatment of absorptive hypercalciuria type I with recurrent calcium oxalate or calcium phosphate nephrolitMasis. 

A. Oxalic acid solutions are highly irritating and corrosive. Ingestion and absorption of oxalate cause acute hypocalcemia resulting from precipitation of the insoluble calcium oxalate salt. Calcium oxalate crystals may then deposit in the brain, heart, kidneys, and other sites, causing serious systemic damage. 

Logic dictates that reducing our calcium intake reduces our risk of kidney stones, so for many years doctors put their kidney stone patients on low-calcium diets. Then some scientists suggested that this could be the wrong approach. They theorized that, if calcium met up with oxalate in the digestive tract, then it would form calcium oxalate there and prevent the absorption of oxalate into the bloodstream. A landmark paper published in the New England Journal of Medicine confirmed this theory. It reported on the discovery that people with a higher calcium intake had a lower risk of kidney stones. 

Hyperoxaluria and occasionally calcium oxalate stones develop in patients with diseases of the ileum or after resection of that portion of the intestine. A number of sophisticated biochemical pathways, all involving overproduction of glycine and glyoxalate, have been invoked to explain the hyperoxaluria. Recently, however, a study from the Hamersmith Hospital in England has suggested that the hyperoxaluria results from increased absorption of oxalate and consequently that it can be readily corrected by reducing oxalate intake in the diet [209]. 

Absorption of calcium may be prevented by the formation of insoluble calcium oxalate where oxalic acid forms a significant proportion of intake. The most notable example is spinach which contains sufficient oxalic acid to render all its calcuim non-available with some to spare for other calcium present in the diet. There is some doubt, however, that this factor has any major effect upon nutrition in normal circumstances. 

Oxalic acid. This compound can inhibit the absorption of calcium because of the formation of calcium oxalate, a relatively insoluble compound. Oxalic acid is high in only a few foods among them, spinach, beet tops, swiss chard, cocoa, and rhubarb. But the amount of oxalic acid present in typical American diets is not sufficiently great to interfere seriously with the absorption of calcium. 

In the past, it was common to restrict dietary calcium in patients with a history of calcium oxalate stones. However, recent data surest that a severe calcium restriction in patients with oxalate stones is not only ineffective but also can lead to bone demineralization. For the prevention of recurrent stone formation, a diet restricted in oxalate, sodium, and animal protein is probably most effective. Only if absorptive hypercalciuria is present should a moderate calcium restriction be imposed. 

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