Oxalate crystals

Two nucleation processes important to many people (including some surface scientists ) occur in the formation of gallstones in human bile and kidney stones in urine. Cholesterol crystallization in bile causes the formation of gallstones. Cryotransmission microscopy (Chapter VIII) studies of human bile reveal vesicles, micelles, and potential early crystallites indicating that the cholesterol crystallization in bile is not cooperative and the true nucleation time may be much shorter than that found by standard clinical analysis by light microscopy [75]. Kidney stones often form from crystals of calcium oxalates in urine. Inhibitors can prevent nucleation and influence the solid phase and intercrystallite interactions [76, 77]. Citrate, for example, is an important physiological inhibitor to the formation of calcium renal stones. Electrokinetic studies (see Section V-6) have shown the effect of various inhibitors on the surface potential and colloidal stability of micrometer-sized dispersions of calcium oxalate crystals formed in synthetic urine [78, 79]. 

Hartel, R.W. and Randolph, A.D., 1986. Mechanisms and kinetic modelling of calcium oxalate crystals in urine-like liquor Part II kinetic modelling. American Institution of Chemical Engineers Journal, 32, 1186-1195. 

Kavanagh, J.P., 1992. Methods for the study of calcium oxalate crystallization and their application to urolithiasis research. Scanning Microscopy, 6, 685-705. 

The presence of particles in the brains of experimental rats and humans exposed to asbestos has been reported (Pontefiart and Cunningham, 1973 Auerbach et al., 1980). In experimental studies, particles of Teflon, a reflux paste, enter the brain via intravascular transport when injected into the bladder (Aaronson et al., 1993). Encephalitic reactions to accumulated calcium oxalate crystals in the brain as a result of infusions of glucose surrogate polyol solutions have been described (PciflPcr etal., 1984). Such studies indicate the capacity of particulates to enter the brain and thus pose a potential pathological threat to the functioning of the central nervous system (CNS). 

A 3-year-old boy consumed a liquid from a container in the family garage He shows central nervous system (CNS) depression, acidosis, suppressed respiration, and oxalate crystals in the urine. Besides supportive and corrective measures, ethanol was administered to the child. 

Tillman-Sutela E, Kauppi A. Calcium oxalate crystals in the mature seeds of Norway spruce, Picea abies (L.) Karst. Trees 1999 13 131-137. 

Contact dermatitis Dumb cane Calcium oxalate crystals... 

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 patients who have ingested more than 30 ml of (pure) methanol or ethylene glycol, dialysis is recommended, and haemodialysis is more effective than peritoneal dialysis. Dialysis both removes the alcohols and their metabolites, and corrects the renal and metabolic disturbances and so is the preferred treatment in severe poisoning. The maintenance dose of ethanol required may be tripled during haemodialysis as ethanol is also removed. Early treatment is indicated if ethylene glycol concentrations are above 20 mg/100 ml (200 mg/1), if the arterial pH is below 7.3, if serum bicarbonate concentrations are less than 20 mM/1, and when there are oxalate crystals in the urine. 

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. 

This is apparently an indirect result of the primary defect in utilization of hydroxypyruvate. It has been suggested that oxidation of glyoxylate by NAD+ is coupled to the reduction of hydroxypyruvate by NADH 366 This and other hyperoxalurias are very serious diseases characterized by the formation of calcium oxalate crystals in tissues and often death from kidney failure before the age of 20. 

The research in this area builds on the earlier work of Haka et al. [57] who found that excised calcifications can be classified into two groups using Raman spectroscopy type I - calcium oxalate dihydrate (cod) and type II - calcium hydroxyapatite (hap). Calcium oxalate crystals are mainly found in benign ductal cysts while calcium hydroxyapatite is found in both carcinoma and in benign breast tissue the chemical specificity of Raman spectroscopy identifies... 

Meric, C. and Dane, F., Calcium oxalate crystals in floral organs of Helianthus annuus L. and II. tuberosus L. (Asteraceae), Acta Biologica Szegediensis, 48, 19-23. 

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. 

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