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

Aims-To investigate whether increasing the daily baseline of gut calcium ca n cause a gradual downregulation of the active intestinal transport of calc ium via reduced parathyroid hormone (PTH) mediated activation of vitamin D, and to discuss why such a mechanism might prevent calcium oxalate rich sto nes. To demonstrate the importance of seasonal effects 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 per iod during a six month crossover study. In a further population of patients on follow up for previous renal stone disease, observations were made on 1 066 24 hour urine samples collected over five years in respect of seasonal effects relevant to the interpretation of the study. Results-In the group of patients on calcium supplements the following resul ts were found. During calcium supplementation, the proportion of urine calc ium to oxalate was higher (increased calcium to oxalate molar ratio), the 2 4 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% PRHudson higher than baseline in the final four wee ks 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 w hile 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 y ears the following results were found. Calcium and oxalate excretion correl ated positively and not inversely. Urine calcium and phosphate excretion we re 5.5% and 2.5% higher, respectively, in "'light" months of the year compa red with "dark" months. A post summer decline in both urine calcium and uri ne phosphate was relevant to the interpretation of the study. Conclusions-Regular calcium supplementation does not raise the product of c alcium and oxalate in urine and the proportion of oxalate to calcium is red uced. 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 regulati ng feedback,loop operating over a period of weeks. In evaluating these mech anisms background seasonal effects are important. It is possible that "prog rammmng" of the gut mucosa in terms of calcium transport is a major determi nant of the relation between calcium and oxalate concentrations in urine an d their relative abundance. Increased oral calcium, in association with a r eduction of the relative proportion absorbed, may be pertinent to the preve ntion of calcium oxalate rich stones.