Calcium oxalate stones: An overview

The master equation:

temporary local toxins + temporary local deficiencies + temporary local excesses = {local medical conditions, temporary or long-lived}


1.Possibly bacteria in the kidney, which may also contribute oxalate as a waste product. Their other waste products may create solubility problems, possibly because of altered pH, particularly too alkaline a urine. They may themselves act as seed crystals or provide seed crystals in their waste products.

2. Many others, possibly including powerful oxidants.


1. B vitamins (especially B6) leading to increased oxalate in urine

2. Magnesium deficiency leading to increased calcium in urine and to increased size of calcium oxalate precipitates.

3. Chelator deficiencies from dietary deficiencies (such as woefully deficient citrus fruit), leading to under-chelated calcium in urine

4. Water deficiencies, leading to too high a solute concentration in urine, leading to larger stones.

5. Antioxidant deficiencies from dietary deficiencies, leading to excessive levels of inappropriately oxidized species.

6. Vitamin C deficiency – leading to too alkaline a urine

7. Many others


1. Calcium over-supplementation at meals, leading indirectly to magnesium deficiency (a portion of dietary magnesium competes with a portion of dietary calcium for active, assisted absorption).

2. Many others.

Another way in which magnesium deficiency aggravates the problem of calcium oxalate stones:

Effect of magnesium on calcium and oxalate ion binding.

Author information

  • 11 Department of Urology, University of Pittsburgh Medical Center , Pittsburgh, Pennsylvania.



Magnesium (Mg(2+)) has been shown to be a kidney stone inhibitor; however, the exact mechanism of its effect is unknown. Using theoretical models, the interactions of calcium and oxalate were examined in the presence of Mg(2+).


Molecular dynamics simulations were performed with NAMD and CHARMM27 force field. The interaction between calcium (Ca(2+)) and oxalate (Ox(2-)) ions was examined with and without magnesium. Concentrations of calcium and oxalate were 0.1 M and 0.03 M, respectively, and placed in a cubic box of length ~115 Angstrom. Na(+) and Cl(-) ions were inserted to meet system electroneutrality. Mg(2+) was then placed into the box at physiologic concentrations and the interaction between calcium and oxalate was observed. In addition, the effect of citrate and pH were examined in regard to the effect of Mg(2+) inhibition. Each system was allowed to run until a stable crystalline structure was formed.


The presence of Mg(2+) reduces the average size of the calcium oxalate and calcium phosphate aggregates. This effect is found to be Mg(2+) concentration-dependent. It is also found that Mg(2+) inhibition is synergistic with citrate and continues to be effective at acidic pH levels.


The presence of magnesium ions tends to destabilize calcium oxalate ion pairs and reduce the size of their aggregates. Mg(2+) inhibitory effect is synergistic with citrate and remains effective in acidic environments. Further studies are needed to see if this can be applied to in vivo models as well as extending this to other stone inhibitors and promoters.

[PubMed – indexed for MEDLINE]

Free PMC Article


Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )


Connecting to %s