The Urinary Excretion of Oxalic Acid in Urolithiasis

Takasaki, Etsuji; Shimano, Eiichiro

doi:10.5980/jpnjurol1928.58.2_210

Cited by 3 publications

(2 citation statements)

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“…Due to the possibility of ethylene glycol toxicity upon presentation, thiamine and pyridoxine were administered as co-factors (27)(28)(29)(30). The role of these co-factors in diethylene glycol toxicity is unknown, but due to the relative safety of these agents in the doses given, we continued this therapy throughout the hospital course.…”

Section: Discussionmentioning

confidence: 97%

Diethylene Glycol: Widely Used Solvent Presents Serious Poisoning Potential

Marraffa

Holland

Stork

et al. 2008

The Journal of Emergency Medicine

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Section: Discussionmentioning

confidence: 97%

Diethylene Glycol: Widely Used Solvent Presents Serious Poisoning Potential

Marraffa

Holland

Stork

et al. 2008

The Journal of Emergency Medicine

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“…As a low, urinary excretion of magnesium may, from a physicochemical viewpoint, be expected to be associated with a reduced inhibitor activity and therefore an increased stone forming propensity, the urinary magnesium has been determined in a number of clinical studies. In general, stone formers appear to have a magnesium excretion not different from that of healthy nonstone forming subjects (1 1,20,26, 32, 40,47,48,52,53). In some studies, however, stone formers were reported to have a low urinary magnesium excretion, either in comparison with controls not matched for age and sex (19, 29, 34), or in comparison with an adequate matched control group (44,50).…”

Section: Magnesium Metabolism In Renal Stone Diseasementioning

confidence: 98%

Magnesium and Renal Stone Disease

Johansson

1982

Journal of Internal Medicine

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Epidemiological aspects of renal stone diseaseRenal stone disease is common in the population with a life time risk between 10 and 20% for males and 3-5% for females. Approximately 50% of unselected stone formers will experience stone recurrence within ten years. Recurrences are particular common in individuals with early onset of the disease and in those with a family history of renal stones (33). A high urinary excretion of calcium, oxalate, uric acid, a high urinary pH, a low urinary volume and low urinary excretion of glycosaminoglycans are risk factors for stone formation and a combination of these risk factors will ultimately define the risk of forming stone (42). The renal stone disease has been proposed to be largely a disease of the affluent society (42). Physico-chemical aspectsThe main part of the stones formed in the kidneys are composed of calcium oxalate, calcium phosphate or a mixture of both. Currently there are three main theories of probable importance in the formation of renal calcium stones: a) the concentration of precipitating substances, mainly calcium, oxalate and phosphate and the solibility of the mineral phace formed; b) the role of urinary promotors of crystallization and crystal aggregation in the urine and c) the role of inhibitors of crystallization and crystal aggregation (14).The urine from most stone formers is supersaturated with respect to calcium oxalate or cald-um phosphate. As the degree of supersaturation varies there is a great overlap between stone formers and none-stone forming subjects. Much attention has been directed to distinguish between these two groups. Subjects without renal stone disease excrete no or only individual crystals in the urine whereas stone formers excrete greater amounts of crystals and, in addition, tend to excrete large aggregations of crystals (41). The main inhibitors of the crystal formation of calcium oxalate and calcium phosphate are citrate, pyrophosphate and magnesium, whereas glycosaminoglucans besides citrate and pyrophosphate play the primary role for inhibiting the aggretion of formed crystals in the urine (14).Already in 1929 Greta Hammarsten indicated that magnesium increased the solibility of calcium oxalate in vitro (18). Others have shown that magnesium decreases the incidence of experimental, calcium oxalate stone formation (4, 15, 43). Desmars and Tawashi (8) emphasized the fine kinetic control magnesium exerts on calcium oxalate formation, because of the greater solibility product of magnesium oxalate compared to that of calcium oxalate.The difficulty in evaluation of results obtained from diluted urine is well illustrated by the fact that pyrophosphate has been shown to be the main inhibitor of calcium phosphate crystal formation when measured in 2% urine, whereas pyrophosphate only accounts for about 10% of the inhibitory activity in whole urine (3). This quantitative technique to determine the inhibitors of calcium phosphate precipitation in whole, undiluted urine, demonstrated that magnesium represents 20% of the total inhib...

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Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones

et al. 1976

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Urine excretion of magnesium (Mg), calcium (Ca) and sodium(Na) was studied in patients with renal Ca stones having normal kidney function (n= 60), and in matched controls (n= 60), on a free diet following an overnight fasting period. In some formers, Mg was lower than in normals, whereas Ca was unusually high resulting in a significantly higher molar Ca/Mg ratio (p less than 0.001). 2. In 3 out of 4 stone groups Na excretion was significantly elevated because of reduced tubular reabsorption. In normals, fractional Na excretion varied between 0.44 and 0.54% of endogenous creatinine clearance, whereas it exceeded 1% in the stone patients. Conversely, the molar ratio Na/Ca was equal in all groups. 3. Fasting urinary cyclic AMP was comparable in both populations supporting the assumption that in the majority of patients Ca- or Mg- wasting via urine may not be responsible for secondary hyperparathyroidism. In small selected groups, losses of divalent cations may act in concert, leading to stimulation of the parathyroid glands. 4. Correlations between minerals and Na reveal a close relationship between Na, Ca and Mg in terms of clearance and excretion rate in patients and controls. Fractional Na and Ca excretion are correlated in patients but not in normals. This suggests that in the absence of phosphaturia, factors other than extracellular volume expansion and/or hyperparathyroidism are operative in stone disease. 5. The origin of fasting natriuresis and relative hypercalciuria may be ascribed to a change, as yet not causally identified, in distal tubular Na reabsorption.

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The Urinary Excretion of Oxalic Acid in Urolithiasis

Cited by 3 publications

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Diethylene Glycol: Widely Used Solvent Presents Serious Poisoning Potential

Diethylene Glycol: Widely Used Solvent Presents Serious Poisoning Potential

Magnesium and Renal Stone Disease

Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones

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