30 to 50% of patients with kidney stones have excessive urinary calcium known as idiopathic hypercalciuria. Calcium restriction is usually not indicated, but can influence the condition of the patient in the following ways:

Chronic high calcium intake of up to 2 grams daily in patients with normal vitamin D levels does not significantly increase urinary calcium, presumably because of a parathormone-mediated decrease in 1,25-dihydroxyvitamin D levels which, in turn, decreases the fraction of calcium absorbed.

Despite a low calcium diet, some hypercalciuric patients will continue to have high urinary calcium excretion rates due to overproduction of 25-dihydroxyvitamin D which stimulates bone resorption along with intestinal calcium absorption.

Urinary oxalate increases as dietary calcium is reduced, perhaps because dietary calcium precipitates oxalate in the intestines to form calcium oxalate which is not absorbed thus increasing the risk of calcium oxalate stones.

Hypercalciuria in perimenopausal women with renal calculi and osteoporosis may be due to excessive bone resorption consequent to estrogen deficiency. In that case, estrogen replacement, rather than calcium restriction, is the indicated treatment.

There is evidence that dietary calcium intake may be inversely associated with the risk of kidney stone formation although it is possible that this association is due to the presence of some other protective factor besides calcium. For example, dairy products, a major source of dietary calcium, are also a major source of phosphorus, which may reduce urinary calcium excretion and calcium oxalate supersaturation.

Increased calcium intake in the form of supplements taken with meals may effectively reduce oxalate absorption in patients with malabsorption, yet supplemental calcium, in contrast to dietary calcium, has been found to be associated with a slightly increased risk for kidney stones. This contradiction may be because supplemental calcium is often taken away from meals. Because of this possibility, when calcium supplements are prescribed, they should be taken with meals to coincide with the time of oxalate ingestion.

Magnesium

Kidney stones have repeatedly been produced in magnesium-deficient animals. Total serum magnesium and erythrocyte magnesium levels may be low in recurrent stone formers. 5% of stone formers have hypomagnesiuria, and the urine of over 25% of stone formers has a lowered magnesium to calcium ratio. The hypomagnesiuria appears to be due to inadequate magnesium intake, as magnesium absorption following supplementation appears to be normal.

Phosphorus

In stone formers, urinary phosphorus may be elevated, thus creating the risk of phosphate deficiency. Hyperphosphaturia appears to correlate with urinary calcium levels, there is evidence that patients with idiopathic hypercalciuria excrete excessive phosphate for any given serum calcium concentration.

Loss of phosphate may increase the activation of 1,25-dihydroxyvitamin D. There also appears to be a failure of the kidneys to convert orthophosphate to pyrophosphate.

Supplementation with orthophosphate reduces urinary calcium with reduction in calcium oxalate supersaturation and stone formation. However, unless baseline phosphate levels are low, the reduction in stone formation appears to be limited, especially as compared to other treatments such as alkali citrate or magnesium.

Doctors caution that the nutritional treatment of illness should be supervised by physicians or practitioners whose training prepares them to recognize serious illness and to integrate nutritional interventions safely into the treatment plan.