However, there is no evidence that a reduction in dietary calcium intake prevents stone recurrence. As urine normally contains much less oxalate than calcium, small increases in urinary oxalate concentration will have a relatively greater effect on calcium oxalate supersaturation than great changes in calcium concentration.
The aim of the present study was to evaluate the urinary excretion of oxalate in calcium stone-forming patients who chronically consumed a low calcium diet, and to examine the effects of an increase in calcium intake on urinary oxalate excretion in normocalciuric and hypercalciuric calcium stone-forming patients. The diagnosis of stone formation was based on a history of colic episodes with expulsion of stones spontaneous or after shock wave lithotripsy and previous or present radiographic evidence of radiopaque stones.
Patients with diseases affecting calcium metabolism primary hyperparathyroidism, hyperthyroidism, acromegaly, sarcoidosis, diabetes, neoplasias, etc. After an initial clinical evaluation, all of them were submitted to a 4-day dietary record. Twenty-two healthy volunteers 9 males and 13 females who had never formed a kidney stone underwent a h urinary oxalate excretion determination as controls. A 4-day dietary assessment could not be obtained for these controls.
Baseline dietary record. During the baseline period, dietary habit was assessed through a 4-day dietary record. Subjects were instructed to keep a daily record describing the amount of each food consumed and not modifying their habitual diet. After the records were received, the same nutritionist evaluated the daily food record during an interview.
Calcium, oxalate and other nutrient intakes were calculated using a computer program 6. For better accuracy, NaCl intake was calculated based on the levels of urinary sodium rather than on the dietary record.
Baseline urinary parameters. A h urine sample was collected on the 4th day of the dietary record to determine calcium, sodium, potassium, creatinine and oxalate. Chronic oral calcium load. The chronic oral calcium load consisted of 1 g of calcium mg bid administered orally at mealtime for 7 days, in addition to their regular diet with the timing of calcium load identical for all groups.
During this period, patients were instructed by the nutritionist to maintain their regular intake of calcium and oxalate to match the intake reported in the first dietary record. Post-load dietary record. A second 4-day dietary record was then obtained from every patient to ensure that the calcium and oxalate intakes of both records were similar, with the calcium supplements being the single difference between the two periods. Subjects who had modified their diet were not included in the study.
Post-load urinary parameters. A h urine sample was collected on the 4th day to determine calcium and oxalate. Urinary oxalate was measured by an enzymatic method 7 based on the oxidation of oxalate by oxalate oxidase followed by measurement of hydrogen peroxide produced during the reaction by a peroxidase-catalyzed reaction using the Sigma Oxalate Diagnostic kit Sigma, St.
The urine samples were acidified below pH 2. Creatinine was measured by the alkaline picrate Jaffe reaction 8 and uric acid by the uricase method 9. Urinary citrate was determined by the citrate-lyase enzymatic reaction Sodium and potassium were measured by flame emission spectrophotometry. Nonparametric tests were used Kruskal-Wallis complemented by the Dunn test to compare the results of all groups. The Wilcoxon test was used to compare results obtained after calcium load versus regular diet in the same group.
Mean urinary parameters obtained under the regular diet and after the calcium load are shown in Table 1. Urinary calcium, sodium, potassium and creatinine levels after calcium load did not differ from those obtained during the regular diet. The 50 calcium stone-forming subjects were classified according to the levels of h urinary calcium on their regular diet and after the calcium load.
Table 2 shows the mean values of calcium, oxalate and sodium chloride intakes obtained from dietary records on the regular diet and after a calcium load. The sodium chloride intake was calculated from h urinary sodium excretion. As a consequence of the supplement given for 7 days, calcium intake was significantly higher compared to the period of regular diet. Oxalate and sodium intake did not change. Table 3 shows mean urinary calcium and oxalate levels on the regular diet and after the calcium load.
Urinary oxalate did not differ between groups. Individual values of urinary oxalate within each group are illustrated in Figure 1. Hyperoxaluria was not observed in the DDHC group. In the past, since increased calcium intake was considered to be an important risk factor for stone formation, calcium restriction was recommended as an obvious intervention to prevent kidney stones in calcium stone-forming patients suffering from hypercalciuria However, this practice has been questioned due to a large epidemiologic study which reported an increased risk for stone formation in subjects consuming a low calcium diet due to secondary hyperoxaluria 5 , although these data had been largely indirect.
Furthermore, several investigators have observed that calcium restriction has a deleterious effect on bone in hypercalciuric patients 12, Calcium also helps reduce its absorption. However, healthy people trying to stay healthy do NOT need to avoid nutrient-dense foods just because they are high in oxalates. Low oxalate diets may help treat some health conditions, including kidney stones.
This article takes a closer look at the low oxalate diet and whether…. Oxalate is a naturally occurring molecule found in abundance in plants and humans. Calcium oxalate crystals in the urine are the most common cause of kidney stones. Learn where they come from, how to prevent them, and how to remove…. Primary hyperoxaluria is a rare disease that leads to kidney and bladder stones. Learn more about causes, symptoms, and what to expect when managing….
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Health Conditions Discover Plan Connect. What is oxalate? Oxalate can reduce mineral absorption. Oxalate may contribute to kidney stones. Does it cause any other problems? Most foods with oxalates are very healthy.
Following gavage of calcium oxalate, the molecule was absorbed intact from one site. Additional calcium was absorbed lower in the gastrointestinal tract after dissociation of the salt. The serum levels of 45 Ca and 14 C are shown for 4 h following IV administration of 0. Levels for both labels were constant in all rats indicating that no loss occurred over the study period. Serum 45 Ca and [ 14 C]-oxalate profiles in a representative rat following intravenous administration of 0.
Data points were connected to show that neither label changed over the time of study. A typical serum 45 Ca and [ 14 C]-oxalate profile following gavage of 0. The pattern of appearance in serum of both 45 Ca and [ 14 C]-oxalate following gavage of the intact salt in all rats showed a steady rise followed by a plateau for both labels until min and then an increase in 45 Ca. The ratio of the two isotopes was constant for the first min. The increase in 45 Ca after min can be explained by absorption from the colon.
Data from the serum appearance of the two tracers could not be fitted by using either of the models developed previously for calcium or oxalate Hanes et al. Data were fitted by adding a delay Compartment 29, Fig. Compartment 27 represented a delay of about min before absorption of calcium from a second site Compartment 26 in the large intestine. Serum 45 Ca and [ 14 C]-oxalate profiles in representative rats following gavage of 0. Model for plasma appearance of 45 Ca-[ 14 C]-oxalate in rat serum following gavage of 0.
Compartment 21 represents plasma. Compartment 29 represents an initial delay prior to absorption from compartment Compartment 24 likely represents the upper intestine and compartment 26 the lower intestine, with compartment 27 a delay compartment between the two absorption sites. Volume of distribution was 50 mL. Figure 3 B shows the typical time course of appearance of 45 Ca and [ 14 C]-oxalate following gavage of 0.
The pattern of appearance of 45 Ca and 14 C from doubly labeled Ca-oxalate was the same with or without the added unlabeled calcium. The pattern of serum appearance of 45 Ca-[ 14 C]-oxalate in the serum of all rats was most consistent with that of soluble 45 Ca at the same molar load and the passive mode of transport via the paracellular route.
The serum profiles of both soluble 45 Ca and insoluble 45 Ca-[ 14 C]-oxalate were markedly different from that of soluble [ 14 C]-oxalic acid, which was absorbed and cleared more rapidly. This indicates the better absorbability in healthy rats of calcium in the soluble form. The appearance in serum of 45 Ca and 14 C-oxalate from the administered 45 Ca-[ 14 C]-oxalate dose was similar for approximately 3 h postdosing, at which time the salt likely reached the colon where colonic bacteria could have dissociated the insoluble 45 Ca-[ 14 C]-oxalate, allowing soluble 45 Ca to be absorbed.
Two absorption scenarios were possible in the small intestine. First, 45 Ca-[ 14 C]-oxalate could have dissociated prior to absorption then reassociated in the blood. Second, 45 Ca-[ 14 C]-oxalate could have been absorbed intact. To determine which of these two scenarios was true, the experiment was repeated with the addition of an equimolar amount of nonlabeled, soluble calcium to the gavage dose. If a small amount of the salt was dissociated in the gut prior to absorption and the moiety was actually absorbed , then the level of appearance of 45 Ca in serum would have been reduced with respect to oxalate because of dilution of 45 Ca in the gut with the added calcium.
Furthermore, the pattern of appearance of the two labels would be expected to differ, with 14 C appearing earlier than 45 Ca as in Fig. However, the pattern of appearance of 45 Ca and 14 C was unaffected by the presence of excess unlabeled calcium Fig. Calcium oxalate was selected for study because it is virtually insoluble and interpretation of label movement in determining a mechanism of absorption would be clearer than for a more soluble salt.
In a previous study in 18 premenopausal women, calcium absorption from calcium oxalate averaged Urinary excretion patterns of 14 C-oxalic acid and Ca-[ 14 C]-oxalate, in the presence and absence of oxalate-rich vegetables, were studied in one human subject Prenen et al. Estimated absorption ranged between 1. Oxalate excretion increased within 1—8 h after ingestion of the labeled meals.
Urinary excretion patterns of 14 C were similar regardless of form or presence of vegetable. However, meals were adjusted to 15 mmol calcium; thus, it is likely that calcium oxalate salt had formed in all meals prior to digestion. This would explain the apparent contrast to our rat data where oxalate absorption was much greater than calcium oxalate absorption.
Although urinary excretion is an inexact approach for determining time of peak absorption, little 14 C was found in the urine after 10 h, suggesting that absorption occurred prior to the colon. In patients with jejunoileal bypass surgery, [ 14 C]-oxalate urinary excretion is elevated, presumably from colonic absorption Hofmann et al. In the rat study, compartmental modeling showed Ca oxalate absorption from two sites in the intestine.
In the colon, it appears that bacterial cleavage of the salt resulted in additional absorption of calcium, but not oxalate. Although calcium appearance in the serum diverged from oxalate after min in all rats, future research at extended time points will be needed to affirm whether or not this is indeed physiological.
Calcium absorption from the human colon was reported Sandstrom et al. In contrast to observations in this study, oxalate was reported to be absorbed from human colon by passive diffusion Binder These studies provide direct, experimental evidence that low molecular weight, neutral, salts such as 45 Ca-[ 14 C]-oxalate are absorbed intact in the whole body rat intestine. These results support the Intact Complex Scheme model proposed by Weaver and Heaney for calcium oxalate absorption and show that calcium does not have to be in soluble form to be absorbed in rats.
Absorption of intact CaCO 3 may explain the ability of subjects with achlorhydria to absorb calcium Recker Moreover, absorption of intact complexes suggests possible therapeutic avenues using small calcium salts for individuals with impaired active calcium transport.
More studies are required to examine candidate calcium salts in models with impaired active transport. Allen H. Calcium bioavailability and absorption: A review. Google Scholar. Andon M. Effect of age, calcium source, and radiolabeling method on whole body 47 Ca retention in the rat. Binder H. Intestinal oxalate absorption. Gastroenterology 67 Bo-Lin G.
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