Relationships between Calcium and Oxalic Acid Intake in the Diet and Their Excretion in the Urine of Normal and Renal-Stone-Forming Subjects

1972 ◽  
Vol 43 (1) ◽  
pp. 91-99 ◽  
Author(s):  
R. W. Marshall ◽  
M. Cochran ◽  
A. Hodgkinson

1. The short-term effects of different intakes of calcium and oxalic acid on the urinary excretion of these substances was studied in eight normal men and eight men with a history of calcium-containing renal stones. 2. The effect of dietary oxalate on urine oxalate depended partly upon the calcium intake. Thus, on a normal calcium intake an increase in oxalate intake caused an increase in oxalate excretion that corresponded to 3·6% of the additional dietary oxalate; on a low calcium diet, however, the increase corresponded to 8·1%. 3. A decrease in daily calcium intake from 1000 to 250 mg caused a fall in calcium excretion averaging 150 mg/day in the patients and 60 mg/day in the controls but this was accompanied by average rises of 10 and 7 mg/day respectively in oxalate excretion, with the result that the calcium oxalate activity products remained almost unchanged. 4. A decrease in oxalate as well as calcium intake resulted in a fall in calcium excretion that was not accompanied by a rise in oxalate excretion, and there was a statistically significant fall in the calcium oxalate activity product in both the patients and normal subjects.

1974 ◽  
Vol 46 (3) ◽  
pp. 357-367 ◽  
Author(s):  
A. Hodgkinson

1. The daily excretion of oxalate, calcium, magnesium and creatinine was determined in fifty-two normal men and sixty-five male patients with calcium oxalate-containing renal stones. 2. Direct relationships were found between calcium and oxalate excretion, magnesium and oxalate excretion and calcium and magnesium excretion in both normal subjects and stone-formers. The significance of these relationships is discussed. 3. The mean excretion of calcium and oxalate was significantly higher in the stone-formers, compared with the controls, both calcium and oxalate excretion being raised by about 20%. 4. The effect of oral ingestion of glucose and casein on the rate of excretion of calcium, magnesium, oxalate and phosphate was examined. Glucose increased the rate of calcium and magnesium excretion but had no effect on oxalate excretion and suppressed phosphate excretion. Casein also increased calcium excretion but had little or no effect on magnesium or oxalate excretion, and it increased phosphate excretion. 5. The association of high calcium excretion with high oxalate excretion, in both normal subjects and stone-formers, results in a high degree of supersaturation of the urine with respect to calcium oxalate. The implication of these findings with respect to the cause and treatment of calcium oxalate stones is discussed.


Author(s):  
Sten Öhman ◽  
Lasse Larsson ◽  
Hans-Göran Tiselius

We analysed calcium, magnesium, oxalate, citrate, urate and creatinine in urine and calculated risk factors in patients who had formed stones composed of calcium oxalate, and calcium phosphate, alone or as a mixture. Patients producing pure calcium oxalate stones (< 0·1% phosphate) had a higher oxalate, and lower calcium excretion than stone-free subjects and patients forming other stone types. In contrast, patients producing calcium oxalate stones containing phosphate, even in trace amounts (> 0·1%) had no increase in oxalate excretion, but a higher calcium excretion than stone-free subjects. We could not correlate any computed variable (e.g. AP(CaOx) index) to stone composition. We conclude that pure CaOx stones may be the result of a high oxalate excretion, and that other calcium containing stones may have another and probably more complex aetiology, including primary precipitation of calcium phosphates.


Author(s):  
J M Brown ◽  
G Stratmann ◽  
D M Cowley ◽  
B M Mottram ◽  
A H Chalmers

Twenty-two recurrent calcium stone formers had 24-h urinary oxalate excretions on their home diets which were significantly greater than those of 30 normal subjects (0·48±0·23 mmol/d; mean±SD compared with 0·31±0·11; P<0·01). The stone formers also demonstrated marked day to day variability in oxalate excretion indicating that a single normal urinary oxalate measurement did not exclude significant hyperoxaluria at other times. On a hospital diet containing 1000 mg calcium per day, urinary oxalate excretion fell significantly from 0·48±0·23 mmol/d to 0·32±0·12; P<0·01. As the urinary calcium excretion in and out of hospital was similar, it seems unlikely that low calcium intake at home was responsible for the hyperoxaluria. All patients had recurrent symptomatic stone disease and had been advised to avoid foods rich in oxalate. Whilst poor compliance is a possible explanation for the variability in oxalate excretion, we believe it is more likely that there is an inadvertent intake of oxalogenic precursors in their diet. As normal subjects do not demonstrate hyperoxaluria on similar home diets, stone formers may have a metabolic defect in the handling of these precursors.


1972 ◽  
Vol 43 (3) ◽  
pp. 433-441 ◽  
Author(s):  
R. W. Marshall ◽  
M. Cochran ◽  
W. G. Robertson ◽  
A. Hodgkinson ◽  
B. E. C. Nordin

1. Diurnal variations in urine calcium oxalate and calcium phosphate activity products were observed in normal men and patients with recurrent calcium oxalate or mixed oxalate—phosphate renal stones. 2. Maximum and minimum calcium oxalate products were higher in the patients than in the controls, the difference being most marked in the patients with calcium oxalate stones. 3. Maximum and minimum calcium phosphate products expressed as octocalcium phosphate [(Ca8H2(PO4)6], brushite or hydroxyapatite, were significantly higher than normal in the patients with mixed stones but not in the patients with calcium oxalate stones. 4. The raised calcium oxalate products in the patients were due mainly to increased concentrations of Ca2+ ions; these, in turn, were due mainly to an increased rate of excretion of calcium. Raised calcium phosphate products were due mainly to hypercalciuria, combined with abnormally high urine pH values. 5. Patients with recurrent calcium stones appear to fall into two types: (1) patients with calcium oxalate stones associated with hypercalciuria, a normal or raised urine oxalate and a normal urine pH; (2) patients with mixed oxalate—phosphate stones associated with hypercalciuria, a normal or raised urine oxalate and a raised urine pH. 6. The implications of these findings in regard to treatment are discussed.


2019 ◽  
Vol 316 (3) ◽  
pp. F409-F413 ◽  
Author(s):  
Tanecia Mitchell ◽  
Parveen Kumar ◽  
Thanmaya Reddy ◽  
Kyle D. Wood ◽  
John Knight ◽  
...  

Dietary oxalate is plant-derived and may be a component of vegetables, nuts, fruits, and grains. In normal individuals, approximately half of urinary oxalate is derived from the diet and half from endogenous synthesis. The amount of oxalate excreted in urine plays an important role in calcium oxalate stone formation. Large epidemiological cohort studies have demonstrated that urinary oxalate excretion is a continuous variable when indexed to stone risk. Thus, individuals with oxalate excretions >25 mg/day may benefit from a reduction of urinary oxalate output. The 24-h urine assessment may miss periods of transient surges in urinary oxalate excretion, which may promote stone growth and is a limitation of this analysis. In this review we describe the impact of dietary oxalate and its contribution to stone growth. To limit calcium oxalate stone growth, we advocate that patients maintain appropriate hydration, avoid oxalate-rich foods, and consume an adequate amount of calcium.


1997 ◽  
Vol 93 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Piergiorgio Messa ◽  
Martino Marangella ◽  
Luisa Paganin ◽  
Mara Codardini ◽  
Aldo Cruciatti ◽  
...  

1. Dietary calcium restriction, an efficient practice in reducing urinary calcium excretion, has been reported to induce either an increase or no change in oxalate excretion, questioning its use in hypercalciuric stone-forming patients. In addition, calcium restriction has been previously demonstrated to induce other urinary changes which might influence the relative supersaturation of calcium oxalate. So the overall effect of calcium deprivation on the relative supersaturation of calcium oxalate is unpredictable. 2. The aim of the study was to evaluate the effect of dietary calcium restriction on the relative supersaturation of calcium oxalate in the urine of stone-forming patients utilizing a computer methodology which takes into account the main soluble complex species of oxalate. 3. We studied 34 stone-forming patients on both a free-choice diet, whose Ca and oxalate content (24 and 1.2 mmol respectively) was assessed by dietary inquiry, and after 30 days on a prescribed low-calcium and normal oxalate diet (11 and 1.1 mmol respectively). Under both conditions, the excretion of the main urinary parameters related to dietary composition, electrolytes, oxalate and daily citrate urinary excretion, were measured. The relative supersaturation of calcium oxalate was calculated by means of an iterative computer method which takes into account the main soluble complex species on which the solubility of calcium oxalate is dependent. In addition, intact parathyroid hormone and 1,25-dihydroxyvitamin D blood levels were also evaluated. In 13 of the patients intestinal calcium absorption was evaluated during both a free- and a low-calcium diet, utilizing kinetics methodology. 4. The low-calcium diet induced, together with an expected reduction of calcium excretion, a marked increase in oxalate urinary output. This finding was independent of the presence or otherwise of hypercalciuria and of the serum levels of parathyroid hormone and vitamin D. Intestinal calcium absorption was also stimulated by calcium deprivation and its levels were well correlated with oxalate excretion. Minor changes in magnesium and citrate excretion were also observed. The overall effect on the relative supersaturation of calcium oxalate consisted in a substantial increase in this parameter during the low-calcium diet. 5. In conclusion, our data reinforce the concept that dietary calcium restriction has potentially deleterious effects on lithogenesis, by increasing the relative supersaturation of calcium oxalate.


1984 ◽  
Vol 67 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Stephen B. Erickson ◽  
Kerry Cooper ◽  
Arthur E. Broadus ◽  
Lynwood H. Smith ◽  
Peter G. Werness ◽  
...  

1. The effect of 1,25-dihydroxyvitamin D [1,25-(OH)2D] on dietary oxalate absorption and postprandial urine supersaturation with calcium oxalate was determined in 11 normal subjects. 2. 1,25-(OH)2D increased the urinary excretion of orally administered [14C]oxalate in the 8 h period after a liquid meal containing 1.875 mmol of calcium and 0.83 mmol of oxalate (P < 0.01), and during a 48 h period when the subjects ingested a diet containing 25 mmol of calcium and 3.3 mmol of oxalate/day (P < 0.01); however, 1,25-(OH)2D administration had no effect on [14C]oxalate excretion when calcium was removed from the liquid meal. 3. 1,25-(OH)2D increased 24 h urinary oxalate excretion from 28.7 ± 2.1 mmol/mol of creatinine to 36.8 ± 2.6 mmol/mol of creatinine (P < 0.05) on the 10 mmol/day calcium diet and from 26.4 ± 2.9 to 33.2 ± 2.2 mmol/mol of creatinine (P < 0.1) on the 25 mmol/day calcium diet. 4. A linear correlation (r = 0.72) was found between plasma 1,25-(OH)2D levels and urinary [14C]oxalate excretion after the liquid meal. 5. 1,25-(OH)2D administration produced postprandial supersaturation of urine with calcium oxalate and calcium oxalate crystalluria. 6. These studies suggest that 1,25-(OH)2D increases oxalate absorption (and urinary excretion) by increasing calcium absorption, which results in less binding of calcium to oxalate in the intestine; therefore more oxalate is available for absorption. The combined effect of increased calcium and oxalate absorption results in postprandial supersaturation of urine with calcium oxalate, with resultant crystalluria.


1989 ◽  
Vol 35 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D M Cowley ◽  
B C McWhinney ◽  
J M Brown ◽  
A H Chalmers

Abstract Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.


Author(s):  
Angela Guerra ◽  
Franca Allegri ◽  
Tiziana Meschi ◽  
Giuditta Adorni ◽  
Beatrice Prati ◽  
...  

AbstractIncreasing urinary volume is an important tool in the prevention of calcium renal stones. However, the mechanism of how it actually works is only partially understood. This study aimed at assessing how urine dilution affects urinary calcium oxalate crystallization. A total of 16 male idiopathic calcium oxalate (CaOx) stone-formers and 12 normal male subjects were studied and 4 h urine samples were taken twice, under low (undiluted urine) and high hydration conditions (diluted urine). An equal oxalate load (1.3mmol/L) was added to both types of urine and the crystallization parameters were assessed. In both stone-formers and normal subjects, the crystallization processes were significantly (p<0.05 or less) more marked in the undiluted urine than in the diluted urine in terms of: a) total quantity of calcium oxalate dihydrate (COD) and calcium oxalate monohydrate (COM) crystals; b) total quantity of crystalline aggregates; and c) aggregation index (i.e., ratio between the area occupied by crystalline aggregates and the area occupied by all the crystals present). The comparison between stone-formers and normal subjects showed that the greatest difference was for the size of COD crystals, which were larger in the urine of the stone-formers. A further important finding was an inverse relationship between changes in urinary volume and in the aggregation index (r=–0.53, p=0.004). In conclusion, urine dilution considerably reduces crystallization phenomena induced in vitro by an oxalate load in both calcium stone-formers and normal subjects.


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