Oxalate stones

Mega vitamin intake of vitamin C may result in diarrhea due to intestinal irritation. Since ascorbic acid is partially metabolized and excreted as oxalate, renal oxalate stones may form in some patients. 

An alternative to thiazides is allopurinol. Some studies indicate that hyperuricosuria is associated with idiopathic hypercalcemia and that a small nidus of urate crystals could lead to the calcium oxalate stone formation characteristic of idiopathic hypercalcemia. Allopurinol, 300 mg daily, may reduce stone formation by reducing uric acid excretion. 

Xylitol is as sweet as sucrose and has been used as a food additive. Because it does not induce formation of dental plaque, it is used as a replacement for sucrose in chewing gum. It appeared to be an ideal sugar substitute for diabetics. However, despite the fact that it is already naturally present in the body, ingestion of large amounts of xylitol causes bladder tumors as well as oxalate stones in rats and mice. Its use has, therefore, been largely discontinued. A possible source of the problem may lie in the conversion by fructokinase of some of the xylitol to D-xylulose 1 -P, which can be cleaved by the xylulose 1-P aldolase to dihydroxy acetone P and glycolaldehyde. 

All adverse reactions appear to be dose-related and resolve with reductions in dose. Two patients developed calcium oxalate stones after 1 year of oral therapy (51). 

Renal Stones Up to 5% of the population are at risk from the development of renal oxalate stones, as a result of both ingested oxalate and that formed endogenously. The process of stone formation is not well understood,... 

A number of reports have suggested that high intakes of vitamin C are associated with increased excretion of oxalate however, much of the oxalate may be the result of nonenzymic formation from ascorbate under alkaline conditions, occurring either in the bladder or after collection, and thus not a risk factor for renal stone formation (Chalmers et al., 1986). Gerster (1997) suggested that people who are recurrent oxalate stone formers should, as a matter of pmdence, restrict their intake of vitamin C to 100 mg per day, but noted that the risk of stone formation in the population at large is inversely related to vitamin C intake. 

Gerster H (1997) No contribution of ascorbic acid to renal calcium oxalate stones. Annals of Nutrition and Metabolism 41, 269-82. 

High doses may cause sleep disturbances, headaches and gut upsets. Ascorbic acid is partly eliminated in the urine unchanged and partly metabolised to oxalate. Doses above 4 g/d, which have been taken over long periods in the hope of preventing coryza, increase urinary oxalate concentration sufficiently to from oxalate stones. Intravenous ascorbic acid... 

Most of the oxalate in the body arises from endogenous sources, rather than the diet. About 40% of the oxalate formed in the body arises from ascorbic acid. About arises from 2-carbon precursors, such as glycine and elhanolamine. Only about 0.1% of the body s glycine is catabolized via oxalate formation. Some people increase their intake of ascorbic acid to levels above the RDA by taking supplements. Consumption of large amounts of ascorbate results in increases in urinary oxalate in some persons but not in others. The normal, basal level of urinary oxalate is about 50 mg/day. The daily intake of 3,0 g of ascorbic acid may double the normal levels of urinary oxalate and thus increase the risk for calcium oxalate stones. 

Roth DA, Breitenfield RV. Vitamin C and oxalate stones. JAMA 1977 237(8) 768. 

Tiselius HG. An improved method for the routine biochemical evaluation of patients with recurrent calcium oxalate stone disease. Clin Chim Acta 1982 122(3) 409-18. 

Benzbromarone causes diarrhea (3-4% of patients), urate and oxalate stones, urinary sand, renal cohc, and allergy in a small number of patients (1). Liver damage, which reverses after withdrawal, has been described (SEDA-18,108). 

Vitamin C Impairment of work at high altitudes Gastrointestinal symptoms Oxalate stones in predisposed persons Possible teratogenesis and carcinogenesis in very high doses... 

An association between the use of 5-ASA in patients with chronic inflammatory bowel disease and the development of a particular type of chronic tubulo-in-terstitial nephritis is difficult to interpret since renal involvement in chronic inflammatory bowel disease may be an extra-intestinal manifestation of the underlying disease [110]. Extra-intestinal manifestations of chronic inflammatory bowel disease are well recognized. The most frequent renal complications are oxalate stones and their consequences such as pyelonephritis, hydronephrosis and on the long-term amyloidosis [111, 112]. As for many drugs, reversible acute interstitial nephritis has been described [90]. 

The main metabolites of ascorbate in the human body are oxalate, dehydroascorbic acid, 2,3-diketogulonic acid, and ascorbic acid 2-sulfate. Of these, oxalate has attracted the most attention because of the potential hazard for renal complications by precipitation of oxalate stones. The above-mentioned metabolic turnover for ascorbate, which appears saturable, indicates that in normal humans the amount of oxalate that can be formed is limited. Therefore, the overall risk of inducing oxalate precipitation by increasing the intake of ascorbate probably is minute. 

A dietary history is important in the evaluation of calcium oxalate stone formers. Patients who are excreting... 

Robertson WG, Peacock M, Heyburn PJ, Hanes FA, Rutherford A, Clementson E, et al. Should recurrent calcium oxalate stone formers become vegetarians ... 

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. 

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. 

Nephrolithiasis occurs in 10% to 25% of patients with gout. Factors that predispose individuals to uric acid nephrolithiasis include excessive urinary excretion of uric acid, an acidic urine, and a highly concentrated urine. The risk of renal calcuh approaches 50% in individuals whose renal excretion of uric acid exceeds 1100 mg/day. In addition to pure uric acid stones, hyperuricosuric individuals are at increased risk for mixed uric acid-calcium oxalate stones and pure calcium oxalate stones. Uric acid stones are usually small, round, and radiolucent. Uric acid stones containing calcium are radiopaque. Uric acid has a negative logarithm of the acid ioiuzation constant of 5.5. Therefore when the urine is acidic, uric acid exists primarily in the un-ionized, less soluble form. At a urine pH of 5.0, urine is saturated at a uric acid level of 15 mg/dL. When the urine pH is 7.0, the solubility of uric acid in urine is increased to 200 mg/dL. In patients with uric acid nephrolithiasis, urinary pH typically is less than 6.0 and frequently less than 5.5. When an acidic urine is saturated with uric acid, spontaneous precipitation of stones may occur. 

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