New in vitro Methodological Approaches to GAG Study in Idiopathic Calcium Lithiasis

Caudarella, Renata; Simonelli, L; Vasi, V.; Rizzoli, Elisabetta; Malavolta, N; Stefani, F. H.; Cappelletti, R

doi:10.1159/000414494

Cited by 3 publications

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“…In 1962 Hodgkinson suggested that a condition of hypocitraturia, defined as a urinary citrate excretion lower than 400 mg/day in males and 200 mg/day in females, may be present in stone formers with urinary tract infection (56). In the last 4 decades numerous work performed both on free or fixed diet conditions, with few exceptions, have described a reduced urinary citrate excretion and/or a hypocitraturia in stone formers when compared with normal subject (19,25,63,128,(134)(135)(136)(137)(138)(139)(140)(141)(142)(143)(144). On the contrary, there is no general agreement on the differences in urinary citrate excretion linked to sex, age and on the incidence of hypocitraturia.…”

Section: Urinary Citrate Excretion and Kidney Stonesmentioning

confidence: 99%

Citrate and mineral metabolism kidney stones and bone disease

Caudarella

Vescini²,

Buffa³

et al. 2003

Front Biosci

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Citrate is a weak acid that is formed in the tricarboxylic acid cycle or that may be introduced with diet. In the present paper all the mechanisms involved in intestinal absorption, renal handling and modulation of citrate will be reviewed. The evaluation of plasma citric acid is scarcely used in the diagnosis of human diseases. On the contrary urinary citrate excretion is a common tool in the differential diagnosis of kidney stones, renal tubular acidosis and it plays also a role in bone diseases. Therefore the importance of hypocitraturia will be reviewed with regard to bone mass, urine crystallization and urolithiasis. Finally particular attention will be paid to the incidence of hypocitraturia and to the therapy with citrate salts, both in kidney stone disease and in osteopenia.

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Section: Urinary Citrate Excretion and Kidney Stonesmentioning

confidence: 99%

Citrate and mineral metabolism kidney stones and bone disease

Caudarella

Vescini²,

Buffa³

et al. 2003

Front Biosci

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Calcium oxalate nephrolithiasis: Defective oxalate transport

Borsatti¹

1991

Kidney International

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Pathogenesis of Idiopathic Calcium Nephrolithiasis: Update 1997

Baggio

Plebani

Gambaro

1998

Critical Reviews in Clinical Laboratory Sciences

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Idiopathic calcium nephrolithiasis (ICN) is a frequent disease in Western countries. The physicochemical theory of lithogenesis, which explains stone formation by the precipitation, growth, and crystalline aggregation of lithogenic salts in the urine, has contributed greatly to the understanding of the pathogenesis of calcium urolithiasis. However, several aspects are still unexplained; the co-existence of familial occurrence, primary tubular dysfunctions with ICN, and anomalies in the systemic handling of oxalate and calcium led to the development of a cellular hypothesis of ICN. A number of cellular defects in the handling of ions has been reported that involves both anion and cation transport. These anomalies are probably the expression of a still unknown cellular defect in idiopathic calcium stone formers. We suggested that an anomaly in the cell membrane composition might be responsible for the complex array of cell ion flux abnormalities observed in ICN. Recently, a disorder in the n-6 polyunsaturated fatty acid series has been described; it is characterized by a lower linoleic acid content and a higher arachidonic acid concentration in both plasma and erythrocyte membrane phospholipids of renal calcium stone patients. This anomaly could cause an increased activity of ion carriers; furthermore, it may lead to increased prostaglandin synthesis and to secondary phenomena at the kidney, skeletal, and intestinal level. As a consequence, critical conditions for lithogenesis in the kidney may ensue. The data suggest a common pathogenesis for hypercalciuria and hyperoxaluria. The systemic defect in the phospholipid arachidonic acid level may be both of dietary or genetic origin; experimental data suggest that the increase in delta-6 desaturase activity, the limiting enzyme in the metabolic pathway of polyunsaturated fatty acids, might be relevant to the pathogenesis of lipid abnormalities observed in nephrolithiasis and to the pathogenesis of ICN and its related problems (at the kidney, intestinal, and bone level).

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New in vitro Methodological Approaches to GAG Study in Idiopathic Calcium Lithiasis

Cited by 3 publications

References 0 publications

Citrate and mineral metabolism kidney stones and bone disease

Citrate and mineral metabolism kidney stones and bone disease

Calcium oxalate nephrolithiasis: Defective oxalate transport

Pathogenesis of Idiopathic Calcium Nephrolithiasis: Update 1997

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