Urinary calcium excretion seems to be influenced by dietary in­takes of calcium, sodium, potassium, protein, and carbohy­drates. However, this relationship was not demonstrated in populations with a low intake of nutrients.


Calcium-load studies conducted by Marshall et al. and Lemann et al. have demonstrated a linear relation between oral assumption and urinary excretion of calcium up to calcium- intake values of 20 mmol/day. Further increases in the intake of calcium involve smaller increases in urinary calcium excre­tion, which become nil with values above 50 mmol/day. In healthy subjects direct measurement showed absorption of a larger fraction of dietary calcium on a low calcium diet (400 mg) than on an high calcium diet (1700 mg) (50 vs 31%) (25). Re­cently Robertson et al. showed that urinary calcium is depen­dent on the logarithm of the calcium intake. Urinary calci­um seem to be abnormally dependant upon dietary calcium in­take in patients with idiopathic hypercalciuria. Intake by calcium supplements should be considered separate­ly from intake by calcium containing foods and beverages be­cause of the different timing of ingestion and the different pat­tern of use.  online canadian pharmacy

In healthy subjects on a standard diet calcium excretion in­creased from 5.44 to 6.42 mmol/day after ingestion of calcium- rich mineral water (339 mg/day calcium) and from 5.60 to 6.91 mmol/day after calcium carbonate supplementation (800 mg/calcium).


Dietary sodium intake can affect markedly the urinary excretion of calcium: an increase of 25 mmol/24 hours in urinary sodium causes an increase of approximately 0.6 mmol/24 hours in uri­nary calcium. Calciuria and natriuria are, indeed, correlated, even though proximal tubular sodium reabsorption does not correlate with calcium reabsorption.


In healthy human subjects dietary habits with a normal intake of NaCl dietary potassium deprivation is associated to an in­crease in urinary calcium excretion togheter with a trend for weight gain.This effect seems to be mediated by sodium and chloride retention and expansion of extracellular volume. In fact, dietary NaCl intake prevents the calciuria of potassium deprivation.


The first observations on the effects of a protein diet on calci­um excretion date back to the twenties, when Sherman et al. observed that an addition of meat to the diet generated an increase in calcium excretion without increasing the absorption of dietary calcium. An increase in urinary calcium excretion af­ter an acute and chronic load of protein was subsequently con­firmed by several Authors.

An explanation for this phenomenon is the endogenous acid load that follows the oxidation of sulphated proteins (methionine, cysteine) with consequent reduction in tubular calcium reabsorp- tion and a state of chronic acidosis, that causes mobilization of calcium from the bone. In parallel, intestinal absorption of calci­um could be enhanced by methionine and lysine load.


The classic observations made by Lemann et al. have shown that an acute load of refined carbohydrates, glucose or saccharose, can cause increased urinary calcium excretion both in lithiasic patients and in healthy controls. Subsequently, Blacklock et al. produced a considerable body of evidence on this subject, confirming the acute and chronic calciuretic effect of glucose and demonstrating that there is a subpopulation of patients with renal calculosis in which the administration of refined carbohydrates leads to a distorted calciuric response, probably linked with an abnormal insulin response.

Hypercalciuria following an acute load of glucose in patients with kidney hypercalciuria has also been confirmed by Pak et al..

The calciuric effect of an oral load of sugar was initially ex­plained by a mechanism of reduced reabsorption of calcium at the level of the distal tubule. More recent studies have shown how glucose can, in dose-dependent mode, en­hance the intestinal absorption of calcium by means of a mech­anism that has not yet been fully defined. Other Authors indicated insulin as the stimulatory mechanism of intestinal calcium absorption.