The GI system of healthy people absorbs magnesium and citrate in order to prevent the oxaltes from producing CaOx crystallization. Unfortunately this is not possible for victims of carbohydrate malabsorption because their gut has been destroyed by pathogens who overgrow due to the availability of undigested carbohydrates. The damaged GI tract is then unable to absorb the magnesium and citrate that are are needed to inhibit CaOx crystallization .

Here is an explanation from about.com

Deficiencies in Protective Factors.
Normally, urine contains protective factors that include magnesium, citrate, pyrophosphate, and various proteins and enzymes. These compounds may protect against stone formation in various ways:

* Allowing salt in the urine to be at higher-than-normal concentrations without forming crystals.
* Preventing crystal formation.
* Coating the crystals and preventing them for adhering to the tube surface.

Deficiencies in these protective substances, therefore, cause stones.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3802507&query_hl=70

1: Clin Chem. 1987 Feb;33(2 Pt 1):243-7.

Chemical factors important to calcium nephrolithiasis: evidence for impaired hydroxycarboxylic acid absorption causing hyperoxaluria.

Cowley DM, McWhinney BC, Brown JM, Chalmers AH.

An investigation of variables important to calcium stone formation in urine indicated significantly increased daily excretion of calcium and oxalate and decreased excretion of ascorbate and citrate by recurrent calcium stone formers. In addition, urine volume, sodium, mucopolysaccharide, and protein were also significantly increased. We compared the uptake of citrate and ascorbate from the gut into the blood in normal controls and stone formers. *These studies indicated significantly depressed absorption of both these hydroxycarboxylic acids in recurrent calcium stone formers. We also found that concurrent administration of citrate inhibited ascorbate absorption and increased urinary oxalate excretion after an ascorbate load in normal subjects and stone formers. These findings suggest a mechanism that explains hyperoxaluria in stone patients on the basis of a malabsorption of citrate, ascorbate, and possibly other hydroxycarboxylic acids.

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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pub
med&dopt=Abstract&list_uids=12474641&query_hl=5

1: Endocrinol Metab Clin North Am. 2002 Dec;31(4):979-99. Related Articles, Links

Stones from bowel disease.

Worcester EM.

Lake Park Dialysis Unit, Division of Nephrology, Department of Clinical Medicine, University of Chicago, 1531 East Hyde Park Boulevard, Chicago, IL 60615, USA. eworcest@medicine.bsd.uchicago.edu

Kidney stones are increased in patients with bowel disease, particularly those who have had resection of part of their gastrointestinal tract. These stones are usually CaOx, but there is a marked increase in the tendency to form uric acid stones, as well, particularly in patients with colon resection. These patients all share a tendency to chronic volume contraction due to loss of water and salt in diarrheal stool, which leads to decreased urine volumes. They also have decreased absorption, and therefore diminished urinary excretion, of citrate and magnesium, which normally act as inhibitors of CaOx crystallization. Patients with colon resection and ileostomy form uric acid stones, as loss of bicarbonate in the ileostomy effluent leads to formation of an acid urine. This, coupled with low urine volume, decreases the solubility of uric acid, causing crystallization and stone formation. Prevention of stones requires treatment with alkalinizing agents to raise urine pH to about 6.5, and attempts to increase urine volume, which increases the solubility of uric acid and prevents crystallization. Patients with small bowel resection may develop steatorrhea; if the colon is present, they are at risk of hyperoxaluria due to increased permeability of the colon to oxalate in the presence of fatty acids, and increased concentrations of free oxalate in the bowel lumen due to fatty acid binding of luminal calcium. EH leads to supersaturation of urine with respect to CaOx, in conjunction with low volume, hypocitraturia and hypomagnesuria. Therapy involves a low-fat, low-oxalate diet, attempts to increase urine volume, and agents such as calcium given to bind oxalate in the gut lumen. Correction of hypocitraturia and hypomagnesuria are also helpful.

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