Calcium oxalate urolithiasis

G6. Gershoff, S. N., and Prien, E. L., Excretion of urinary metabolites in calcium oxalate urolithiasis. The effect of tryptophan and vitamin Bg administration. Am. ]. Clin. Nutr. 8, 812-816 (1960). 

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. 

Khan SR, Shevok PN, Hackett RL. Acute hyperoxaluria, renal injury and calcium oxalate urolithiasis. J.Urol. 1992 147 226-30. 

Marengo, S. R., Chen, D. H., Kaung, H. L., Resnick, M. L, and Yang, L. (2002). Decreased renal expression of the putative calcium oxalate inhibitor Tamm-Horsfall protein in the ethylene glycol rat model of calcium oxalate urolithiasis. J Urol 167, 2192-2197. 

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). 

Lewandowski S, Rodgers AL (2004) Idiopathie calcium oxalate urolithiasis risk factors and conservative treatment. Clin Chim Acta 345 17-34. doi 10.1016/j.cccn.2004.03.009... 

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

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. ... 

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. 

The last theory on stone formation comprises the matrix theory in which proteins may play an important role in urolithiasis (FI). This theory is based on analyses of many stones, which revealed that the core of these stones contained protein. It had been shown in vitro that certain proteins bind calcium and even induce the calcification process (Rl). These proteins, also called promoters, were therefore considered to be able to activate the initial crystallization process. However, these results could not be verified (FI). Recently it has been shown that in vitro calcium oxalate crystals do contain protein and that the crystallization in urine is not a random event, but rather a selective phenomenon (M4). This supports an earlier statement that stones contain about 1.6% of their weight in nondialyzable extractable protein and that the composition is the same for all stones, regardless of their mineral composition (S7). 

Hyperuricosuria is a major etiological factor in uric acid lithiasis. In addition, there is evidence for an etiological role of hyperuricosuria in calcium oxalate stone formation (1,2). Indeed, in our stone clinic, a high proportion of hyperuricosuria was also noticed among the patients with calcium urolithiasis. Since the hyperuricosuria in our stone clinic patients was established on the basis of urate determination on urine collections obtained on a regular home diet, the possibility of dietary hyperuricosuria was raised. We have therefore evaluated the contribution of dietary purine intake to uric acid excretion in our stone patients under controlled dietary conditions. 

Robertson, W.G., Knowles, F., Peacock, M., Urinary acid mucopolysaccharides inhibitors of calcium oxalate crystallization. In Urolithiasis Research. Eds. Fleisch, H., Robertson, W.G., Smith, L.H., Vahlensieck, W., Plenum Press - New York and London 1976, pp. 331-334. 

Robertson, W.G., F. Knowles, M. Peacock Urinary Acid Mucopolysaccharide Inhibitors of Calcium Oxalate Crystallisation. Urolithiasis Research (Eds. H. Fleisch, W.G. Robertson, L.H. Smith, W. Vahlensieck) New York-London, Plenum Press, p. 331,1976. 

Approximately 10% of the human population (with regional differences indicating both genetic and environmental factors [33]) is affected by the formation of stones or calculi in the urinary tract. Urolithiasis is not only a painful condition, but also causes annual costs to the health system in the order of billions of dollars in the USA alone [34, 35]. Based on their composition, structure and location in the urinary tract, renal stones have been classified into 11 groups and their formation mechanisms have been discussed together with alterations in urinary parameters and metabolic risk factors for renal lithiasis [35]. Approximately 70% of these stones contain calcium oxalate monohydrate (COM) and dihydrate as major components, while other calculi are composed of ammonium magnesium phosphate (struvite), calcium phosphates (hydroxyapatite and brushite), uric acid and urates, cystine and xanthine. An accurate knowledge of the solubilities of these substances is necessary to understand the cause of renal or bladder calculi formation and find ways towards its prevention and treatment [36]. 

Inhibition of nucleation has been investigated for a range of different crystallization phenomena, most notably for calcium carbonate crystallization with the aim of preventing fouling [8,13,14], crystallization of calcium oxalate with a view to understanding possible mechanisms for preventing urolithiasis (kidney stone formation) [15,16], crystallization of salts from well waters (prevention of well blockage in oil and gas exploitation [17], and sea water desalination [18]. 

Secondary-enteric-hyperoxaluria is a typical complication in patients with diseases involving fat malabsorption, e.g., cystic fibrosis, chronic inflammatory bowel diseases (Crohn s disease), and short-bowel syndrome (Hoppe et al. 1998 Karlowicz and Adelman 1998 SiDHuetal. 1998). Normally, oxalate is intestinally bound to calcium to form insoluble calcium oxalate, which is not absorbed. In patients with enteric hyperoxaluria, calcium instead binds to fatty acids, so more soluble oxalate is absorbed (Williams and Wandzilak 1989). Secondly, patients with cystic fibrosis lack intestinal oxalatedegrading bacteria, Oxalobacter formigenes, which will increase free and absorbable intestinal oxalate (SiDHU et al. 1998). Up to 50% of our patients with cystic fibrosis have hyperoxaluria and nearly 15% develop urolithiasis or NC (Hoppe et al. 2005). Enteric hyperoxaluria may also lead to progressive NC and/or recurrent urolithiasis (Neuhaus et al. 2000). 

Schwille PD, SchmiedI A, Herrmann U, Fan J, Gottlieb D, Manoharan M, Wipplinger J (1999) Magnesium, citrate, magnesium citrate and magnesium-alkali citrate as modulators of calcium oxalate crystallization in urine observations in patients with recurrent idiopathic calcium urolithiasis. Urol Res 27 117-126... 

Cohanim M, Yendt ER. Reduction of urine oxalate during long-term thiazide therapy in patients with calcium urolithiasis. Invest Urol 1980 18 170-173. 

Urinary oxalate plays a crucial role in urolithiasis, primarily due to the extremely low solubility of its calcium salt. This may lead to crystalluria, urolithiasis and nephrocalcinosis. The pathology of oxalate in humans can be divided into three principal groups ... 

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