Oxalate crystal deposition

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. 

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. 

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. 

Gardner TB, Manning HL, Beelen AP, Cimis RJ, Cates JM, Lewis LD. Ethylene glycol toxicity associated with ischemia, perforation, and colonic oxalate crystal deposition. J Chn Gastroenterol 2004 38(5) 435-9. 

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... 

Urinary tract Vitamin C can rarely cause nephrotoxicity due to oxalate crystal deposition. This can be fatal, as in the case of a patient who chose to forgo treatment and failed to disclose his use of high-dose vitamin C intra-renal oxalate crystal deposition was demonstrated at autopsy [37 ]. 

Add a little caustic potash solution. Crystals of potassium oxalate are deposited. The ester is hydrolysed. 

Ethylene glycol, an industrial solvent and an antifreeze compound, is involved in accidental and intentional poisonings. This compound is initially oxidized by alcohol dehydrogenase and then further biotransformed to oxalic acid and other products. Oxalate crystals are found in various tissues of the body and are excreted by the kidney. Deposition of oxalate crystals in the kidney causes renal toxicity. Ethylene glycol is also a CNS depressant. In cases of ethylene glycol poisoning, ethanol is administered to reduce the first step in the biotransformation of ethylene glycol and, thereby, prevent the formation of oxalate and other products. 

Three stages of ethylene glycol overdose occur. Within the first few hours after ingestion, there is transient excitation followed by CNS depression. After a delay of 4-12 hours, severe metabolic acidosis develops from accumulation of acid metabolites and lactate. Finally, delayed renal insufficiency follows deposition of oxalate in renal tubules. The key to the diagnosis of ethylene glycol poisoning is recognition of anion gap acidosis, osmolar gap, and oxalate crystals in the urine in a patient without visual symptoms. 

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. 

Parenteral naftidrofuryl was withdrawn from the market following reports of severe adverse effects with intravenous or intra-arterial bolus injections, including intracardiac conduction defects, epileptic seizures, severe anaphylactic reactions, and acute renal insufficiency secondary to deposition of oxalate crystals in the tubules (SED-12, 473) (SEDA-17, 244). 

A 23-year-old man developed acute renal insufficiency due to hyperoxaluria and intratubular deposits of oxalate crystals after attempting suicide with an overdose of piridoxilate (SEDA-11,180). 

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). 

Metabolism of ascorbic acid can lead to deposition of oxalate crystals in kidney tissue. Reduction of carcinogenic Cr(VI) by ascorbic acid generates as-corbate-Cr(III)-DNA cross-links that have been linked to mutagenicity and the formation of DNA lesions. Uranyl acetate-ascorbate has also been shown to nick plasmid DNA. 

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. 

Renal pelvis or tubules Crystal deposition Oxalate Indinavir Sulfonamides Acyclovir Tumor lysis syndrome... 

To a solution of 13.2 g (0.05 mole) of sodium cis,c/s-diamminecarbonato-dicyanocobaltate(III) dihydrate in 100 mL of water is added 25 mL of 30% perchloric acid dropwise in an ice-bath until the evolution of carbon dioxide ceases. To the resulting solution is added 18 g (0.10 mole) of potassium oxalate dihydrate, and the mixture is then stirred at 40° for four hours. The solution is filtered after neutralization with a 6 mole/L potassium hydroxide solution, and the filtrate is charged on an ion-exchange column containing Dowex 1-X8 resin in the Cr form (100-200 mesh, 4 cm x 30 cm). After the column has been washed with water, the elution is started with a 0.1 mole/L sodium chloride solution. Only one yellow band descends. The effluent is collected and concentrated to 10 mL, and then filtered to remove the deposited sodium chloride. After keeping the filtrate in a refrigerator, yellow crystals deposit. The crude product is recrystallized from the minimum amount of warm water ( 50°). The crystals are collected on a filter, washed with cold water, ethanol, and diethyl ether, and finally dried under vacuum. The yield is about 3 g. Anal. Calcd. for Na[Co(CN)2(ox)(NH3)2]-2H20 C, 16.45 H, 3.45 N, 19.18. Found C, 16.61 H, 3.37 N, 19.13. 

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. 

Unfortunately nephrolithiasis is a recirrrent disease and about 75% of patients suffer the recurrence within 10 years. Therefore it is important to develop new more efficient preventative therapies, which can inhibit the formation of kidney stones or possess properties of dissolution of calciitm oxalate deposits. The possible approach constitutes modeling the potential inhibitors forming calcium oxalate crystals. On the other hand there are available compoimds directly influencing the calciiun oxalate formation (inhibitory or dissolution effect) e.g. citrate. It should be noted that compounds possessing dissolution properties of calcimn oxalate carmot interfere too much into the whole calcimn economy. 

Suberin is laid down in the cell wall of calcium oxalate crystal idioblasts. This deposition has been characterized in crystal cells in the bark of Larix decidua, Acacia Senegal, and Picea abies (481, 482). The suberin in crystal idioblast cell walls from Agave americana was characterized both ultrastructurally (Fig. 6.4.3) and chemically, and the major aliphatic component was shown to be octadocenedioic acid (25%) (117). The basal walls of leaf trichomes are suberized as shown in Abutilon megapotamicum (161), Ananas comosus (395), and Larrea tridentata (451). The walls of oil cells found in Acorus calamus (9) and Laurus nobilis (291) also appear ultrastructurally to be suberized. Suberized cells encircle silica cells in the stem of Lolium temulentum (271). In all of the cases listed above, the suberin may serve to protect the rest of the plant from potentially toxic components. 

PH I is characterized by a highly elevated urinary excretion of oxalate and glyoxylate (>0.8 mmol/ 1.73m body surface area per day, normal <0.5). The urine is saturated with respect to calcium oxalate, which causes renal calculi, (medullary) NC, or both. With disease progression and declining renal function, calcium oxalate crystals are deposited in the parenchyma of other organs, as well as in bones and the retina (Leumann and Hoppe 2001). 

In the case of human exposure to ethylene glycol, oxalic acid was found to be the end-product of metabolism. It precipitated to crystals of calcium oxalate monohydrate in the tubular lumen, causing acute kidney injmy with extensive intracellular intraluminal crystal depositions, and subsequently acute oxalate nephropathy. ... 

The b.p. under diminished pressure has been given as 80-81°/18 mm. To obtain a very pure sample of the amine, dissolve 1 part (by weight) of the above product with a sohitiuii of 1-04 parts of crystallised oxalic acid in 8 parts of hot water, add a little deculeiirisiiig carbon, and tilter. The liltered solution deposits crystals uf the acid oxalate about o g. of tliis salt remains in each 100 ml. of... 

If very pure amine is desired the product described above is dissolved with 1.04 parts of crystalline oxalic acid in eight parts of hot water. After clarification with Norite, the filtered solution on cooling deposits crystals of the acid oxalate. About 5 g. of the salt remains in each 100 cc. of the mother liquor most of this can be obtained by evaporation and further crystallization. The amine is liberated from the pure oxalate with potassium hydroxide, distilled with steam, and purified as described above. When a known amount of amine is desired in water solution (as for optical resolution) a weighed amount of the (anhydrous) oxalate is decomposed and the amine is distilled quantitatively with steam. 

To this acid was then added 1 g of 4-ethyl-2,3-dioxo-1-piperazinocarbonyl chloride (from the reaction of N-ethylethylenediamine and diethyl oxalate to give 2,3-dioxo-4-ethyl-piperazine which Is then reacted with phosgene) and the resulting mixture was reacted at 15°C to 20°C for 2 hours. After the reaction, a deposited triethylamine hydrochloride was separated by filtration, and the filtrate was incorporated with 0.4 g of n-butanol to deposit crystals. The deposited crystals were collected by filtration to obtain 1.25 g of white crystals of 6-[ D(—l-Ct-(4-ethyl-2,3-dioxo-1 -piperazinocarbonylaminolphenylacetamido] penicillanic acid. Into a solution of these crystals in 30 ml of tetrahydrofuran was dropped a solution of 0.38 g of a sodium salt of 2-ethyl-hexanoic acid in 10 ml of tetrahydrofuran, upon which white crystals were deposited. The deposited crystals were collected by filtration, sufficiently washed with tetrahydrofuran and then dried to obtain 1.25 g of sodium salt of 6-[D(—)-a-(4-ethyl-2,3-di-0X0-1-piperazinocarbonylaminolphenylacetamido] penicillanic acid, melting point 183°C to 185°C (decomposition), yield 90%. 

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