Why oral calcium supplements may reduce renal stone disease: report of a clinical pilot study

Abstract

Aims-To investigate whether increasing the daily baseline of gut calcium can cause a gradual downregulation of the active intestinal transport of calcium via reduced parathyroid hormone (PTH) mediated activation of vitamin D, and to discuss why such a mechanism might prevent calcium oxalate rich stones. To demonstrate the importance of seasonal eVects upon the evaluation of such data. Methods-Within an intensive 24 hour urine collection regimen, daily calcium supplementation (500 mg) was given to five stone formers for a 10 week period during a six month crossover study. In a further population of patients on follow up for previous renal stone disease, observations were made on 1066 24 hour urine samples collected over five years in respect of seasonal eVects relevant to the interpretation of the study. Results-In the group of patients on calcium supplements the following results were found. During calcium supplementation, the proportion of urine calcium to oxalate was higher (increased calcium to oxalate molar ratio), the 24 hour urine product of calcium and oxalate did not rise, and urine oxalate was lower during the first six weeks of supplementation. Twenty four hour urine calcium was 10.2% higher than baseline in the final four weeks of the 10 weeks of supplementation. Twenty four hour urine phosphate was 11.4% lower during the first six weeks of supplementation, but then rose while the patients were still on supplementation; renal tubular reabsorption of phosphate (TmP/GFR) mirrored the urine phosphate changes inversely. PTH was higher after stopping supplementation, but 1,25-(OH) 2 -cholecalciferol changes were not detected. In the 1066 urine samples collected over five years the following results were found. Calcium and oxalate excretion correlated positively and not inversely. Urine calcium and phosphate excretion were 5.5% and 2.5% higher, respectively, in "light" months of the year compared with "dark" months. A post summer decline in both urine calcium and urine phosphate was relevant to the interpretation of the study. Conclusions-Regular calcium supplementation does not raise the product of calcium and oxalate in urine and the proportion of oxalate to calcium is reduced.The underlying mechanisms of the changes seen in phosphate, calcium, and PTH and the observations on 1,25-(OH) 2 -cholecalciferol are not clear. Observed changes in phosphate could possibly be part of a calcium regulating feedback loop operating over a period of weeks. In evaluating these mechanisms background seasonal eVects are important. It is possible that "programming" of the gut mucosa in terms of calcium transport is a major determinant of the relation between calcium and oxalate concentrations in urine and their relative abundance. Increased oral calcium, in association with a reduction of the relative proportion absorbed, may be pertinent to the prevention of calcium oxalate rich stones. (J Clin Pathol 2001;54:54-62)

Potassium‐sodium citrate prevents the development of renal microcalculi into symptomatic stones in calcium stone‐forming patients

“…In the present study, we compared male and female patients who did not receive any citrate therapy (non‐citrate group, n = 157) with those who received KNa‐cit (citrate group, n = 60); KNa‐cit was administered at 3000 mg/day (K‐cit, 463 mg/100 mg; Na‐cit, 390 mg/1000 mg). All patients were counseled by outpatient clinical urologists and dieticians to increase fluid intake to >2 L/day, and to eat moderately low‐salt (6 g/day, maximum) meals containing more than 600–1000 mg/day of calcium, based on a previous report . The non‐citrate group did not receive any medical treatment.…”

Mineral water fortified with folic acid, vitamins B6, B12, D and calcium improves folate status and decreases plasma homocysteine concentration in men and women

“…In the study of Kawano et al (1998), 1 g of calcium carbonate increased urinary calcium excretion by 1.3 mmol (27%). In the study of Williams et al (2001), 500 mg calcium carbonate increased calcium excretion 0.96 mmol (10.2 %), and in the study of Fardellone et al (1998), 1200 mg of calcium increased calcium excretion by 1.4 mmol/l (39%). Increase in urinary calcium excretion has been considered as a surrogate marker of calcium absorption.…”

Do Oral Calcium Supplements Increase the Risk of Urolithiasis?

“…Increased calcium intake through diet or taking supplements, increases urinary excretion of calcium [16,18]. Therefore, one might expect an increase in risk of stone formation.…”

“…There is a paucity of data in this group; the two most relevant studies are described in a small prospective study of eight stone formers (only five of whom completed the study) with either hypercalciuria or hyperoxaluria, one calcium carbonate supplement (containing 500 mg calcium) was taken in the morning for 10 weeks [18]. Urinary calcium increased whilst urinary oxalate decreased, resulting in an increased calcium to oxalate ratio and no increase in the product of calcium and oxalate, leading to a theoretical reduction in risk of stone formation.…”