Calcium oxalate deposition

In the rare hereditary disease essential pentosuria, considerable quantities of L-xylulose appear in the urine because of absence of the enzyme necessary to reduce L-xylulose to xyhtol. Parenteral administration of xylitol may lead to oxalosis, involving calcium oxalate deposition in brain and kidneys (Figure 20-4). Various drugs markedly increase the rate at which glucose enters the... 

Ethylene glycol poisoning can canse acidosis, central nervous system depression, pulmonary edema, acute oliguric renal failure with crystalluria, liver damage due to calcium oxalate deposition, nausea, abdominal pain, and cramping, acute colonic ischemia (29), and papilledema and abducens nerve palsy (30). 

The terminology used to describe conditions associated with prominent renal calcium deposits dismisses the importance of the phosphate anion. Renal parenchymal injury with prominent calcium oxalate deposition is referred to as oxalate nephropathy. Oxalate nephropathy is seen in the setting of primary hyperoxaluria or enteric hyperoxaluria secondary to fat malabsorption. Renal parenchymal injury with abundant calcium phosphate deposits is referred to as... 

Pinheiro El, Camara N, Osaki K, De Moura E, Pacheco-Silva A. Early presence of calcium oxalate deposition In kidney graft biopsies Is associated with poor long-term graft survival. Am.J.Transplantatlon 2005 5 323-9. 

Primary hyperoxaluria has been defined by Archer et al. (A7, A9) as a clinical entity characterized by progressive calcium oxalate urolithiasis and nephrocalcinosis beginning in early childhood. It might be associated with disseminated extrarenal calcium oxalate deposits, a condition known as oxalosis (A7) it is not known whether oxalosis always represents a stage in the natural history of primary hyperoxaluria (S9). 

There is little reported information on industrial exposure, although chronic inflammation of the upper respiratory tract has been described in a worker exposed to hot vapor arising from oxalic acid. Ingestion of as little as 5 g has caused fatalities there is rapid onset of shock, collapse, and convulsions. The convulsions are thought to be the result of hypocalcemia due to the calcium-complexing action of oxalic acid, which depresses the level of ionized calcium in body fluids. Marked renal damage from deposition of calcium oxalate may occur. A study of railroad car cleaners with heavy exposure to oxalic acid solutions found an increased incidence of urinary stones. There was a 53% incidence of urolithiasis in exposed workers compared with a rate of 12% in unexposed workers from the same company. ... 

Clinical manifestations occur in three phases. In the neurological stage, the patient appears intoxicated, with slurred speech, ataxia, stupor, and hallucinations, and may be comatose, with respiratory depression. The cardiopulmonary stage is delayed by 12-24 hours, when hypotension, tachycardia, muscle tenderness and congestive cardiac failure are seen. After 1-3 days the renal stage supervenes, with loin pain, crystalluria, oliguria and renal failure, as a result of calcium oxalate crystal deposition in the renal tract. Sequestration of calcium can cause profound hypocalcaemia, tetany, and cardiac arrhythmia. 

For example, normal urine is supersaturated with calcium oxalate. To prevent formation of renal calculi (stones)719 an inhibitory glycoprotein is present and slows the formation and growth of crystals.720 Under some disease conditions calcium carbonate stones may form in pancreatic ducts. A17 kDa lectinlike glycoprotein called lithostatine has been proposed to inhibit stone formation by binding to certain planes on CaC03 microcrystals just as antifreeze proteins (Box 4-D) inhibit ice formation.721 However, this proposed function for lithostatine is doubtful.722 723 Pathological deposits of crystalline calcium pyrophosphate and basic calcium phosphates are sometimes present in joints,724 even in Neanderthal skeletons.725... 

Kidney failure from the metabolic formation of calcium oxalate has been especially common in cat species, which have voracious appetites for ethylene glycol in antifreeze. Deposits of solid calcium oxalate have also been observed in the liver and brain tissues of victims of ethylene glycol poisoning. 

Allopurinol is used in the treatment of hyperuricemia, which is associated with chronic gout and in cancer chemotherapy. Allopurinol has been used in renal calculi caused by the deposition of calcium oxalate and of 2,8-dihydroxy-adenine. Allopurinol treatment does cause hypersensitivity reaction, which may be fatal. 

Bark contains 2-5% inorganic solids of the dry bark weight (determined as ash). The metals are present as various salts including oxalates, phosphates, silicates, etc. Some of them are bound to the carboxylic acid groups of the bark substance. Calcium and potassium are the predominating metals. Most of the calcium occurs as calcium oxalate crystals deposited in the axial parenchyma cells. Bark also contains trace elements, such as boron, copper, and manganese. 

Some precipitates are deposited slowly and the solution is in the state of supersaturation for a considerable time. Thus, when calcium oxalate is precipitated in the presence of larger amounts of magnesium ions, the precipitate is practically pure at first, but if it is allowed to remain in contact with the solution, magnesium oxalate forms slowly (and the presence of calcium oxalate precipitate tends to accelerate this process). Thus, the calcium oxalate precipitate becomes contaminated owing to post-precipitation of magnesium oxalate. Post-precipitation often occurs with sparingly soluble substances which tend to form supersaturated solutions, they usually have an ion in common with the primary precipitate. Another typical example is the precipitation of copper or mercury(II) sulphide in dilute acid solution, which become contaminated, if zinc ions are present, by post-precipitation of zinc sulphide. Zinc ions alone may not be precipitated with sulphide ions under identical circumstances. 

Disposition in the Body. Ethylene glycol is metabolised initially to glycoaldehyde and subsequently to lactic acid and oxalic acid. Calcium oxalate crystals are deposited in the kidneys and some oxalate may be excreted in the urine together with unchanged ethylene glycol. 

Arnott H. J. and Webb M. A. (1983) The structure and formation of calcium oxalate crystal deposits on the hyphae of a wood rot fungus. Scan. Electr. Micros. 3, 1747-1750. 

Calcium and oxalate arc closely associated with the fomiation of stones in the urinary tract. Kidney stones (renal calculi) and bladder stones are mineral deposits containing protein. They can have a diameter of a centimeter or greater. Most kidney stones (75%) are composed mainly of calcium oxalate or calcium oxalate with hydroxyapatite. Uric acid stones account for about 10% of stones xanthine stones are rare. Calcium containing kidney stones occur in fetem nations and affect about one person in 1000. The disease may occur in children, but typically occurs after rhe age of 30 and in men, Calcium biadder stones occur malniy in the children of underdeveloped countries, such as Thailand, and occur rarely in West em nations. Some kidney stones do not result in symptoms. Others may cause blood loss in the urine. Stones that obstruct the flow of urine from the kidney into the ureter result in violent pain, nausea, and vomiting. 

Eroberg K, Dorion RP, McMartin KE. The role of calcium oxalate crystal deposition in cerebral vessels during ethylene glycol poisoning. Clin Toxicol (Phila). 2006 44 315-358... 

Renal parenchymal calcium deposition can be associated with significant renal dysfunction. When calcium deposits are encountered on renal biopsy, the calcium salt typically contains either phosphate or oxalate. The two anions are easily differentiated pathologically, as calcium oxalate is identified as refractile crystals under polarized light. In contrast, calcium phosphate is non-polarizable but gives a positive histochemical reaction to the von Kossa stain [16]. 

Arranged horizontally or radially in the tree are the wood rays, which, as mentioned earlier, are composed predominantly of small, bricklike, and often living cells called parenchyma see Figures 4, 7, and 11). These cells function in radial translocation but have a major role as a storage receptacle, and frequently contain extraneous materials such as starch, fats, oils, various sugars, and inorganic depositions such as calcium oxalate crystals or silica (Figure 12). 

Chronic megadoses of vitamin C may precipitate formation of calcium oxalate renal stones, oxalate nephropathy, and renal failure. The amount required to cause this is variable from 2 to 8gday . Bone oxalate deposits have also been reported. Esophageal and dental erosion are possible with tablet ingestion. Heinz body hemolytic anemia has been seen in premature infants. 

Animals may develop subacute toxicity if enough plant material is ingested to produce hypocalcemia and kidney damage, but no so much that the animal dies. With larger or more prolonged exposures, animals may experience larger deposits of calcium oxalate crystals that result in renal fibrosis or renal failure which can ultimately lead to death. 

Larger particles can also be obtained by controlling pH, provided the solubility of the precipitate depends on pH. For example, large, easily filtered crystals of calcium oxalate are obtained by forming the bulk of the precipitate in a mildly acidic environment in which the salt is moderately soluble. The precipitation is then completed by slowly adding aqueous ammonia until the acidity is sufficiently low for removal of substantially all of the calcium oxalate. The additional precipitate produced during this step deposits on the solid particles formed in the first step. 

Calculate the concentrations of H3O+, OH-, HSe04-, and Se04 - in 0.12 M H2Se04, selenic acid, solution. Some kidney stones are crystalline deposits of calcium oxalate, a salt of oxalic acid, (COOH)2. Calculate the concentrations of H3O+, OH-, COOCOOH-, and (C0Q-)2 in 0.12 M (COOH)2. Compare the concentrations with those obtained in Exercise 62. How can you explain the difference between the concentrations of... 

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