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Here is an explanation from about.com
The key process in the development of kidney stones is supersaturation.
* This process involves salts that are carried in
urine. Such salts may include calcium oxalate, uric
acid, cystine, or xanthine.
* These salts can become extremely concentrated
under certain circumstances: if the volume of urine is
significantly reduced; or if abnormally high amounts
of crystal-forming salts are present.
* When concentration levels reach the point at
which the salts no longer dissolve, they precipitate
out and form crystals.
Different factors may be involved in either reducing urine volume or increasing the levels of the salts.
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Researchers believe that another symptoms of Crohn's and colitis also increase oxalate absorption. They believe that the loss of bicarbonate in the liquid stool negatively impacts the patient and increases the oxalate solubility
I am quoting from one research article:
"Malabosorption associated with ileal disease[Crohn's and colitis] causes increased oxalate absorption by increasing oxalate solubility in the intestinal lumen and permeability of the colonic mucosa; a reduced citrate excretion is associated in relation to mild acidosis due to the loss of bicarbonate in the liquid stool. In ulcerative colitis, especially if an ileostomy is present, urine are scanty and concentrated, and urine pH falls, leading to uric acid or mixed stones."
Here is another article that explains how the problems( including malabsorption) of IBD can cause high oxalates.
"Loss of water and salt in diarrheal stool leads to decreased urine volumes. The low voluume decreases the solubility of uric acid, causing crystallization and stone formation."
Since the inability to digest certain carbohydrates causes most cases of Crohn's and colitis,avoiding these carbohydrates by implementing SCD would stop the symptoms of IBD and prevent the crystallization and stone formation.
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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?
cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12161938&query_hl=2
1: Arch Ital Urol Androl. 2002 Jun;74(2):61-4. .
Urinary patterns of patients with renal stones associated with chronic inflammatory bowel disease..
Trinchieri A, Lizzano R, Castelnuovo C, Zanetti G, Pisani E..
Institute of Urology, IRCCS Ospedale Maggiore, Milano, Italy. uropoli@mailserver.unimit.it.
OBJECTIVE: The aim of this study was to analyze the frequency of renal stone patients with chronic inflammatory bowel disease and their urinary patterns. METHODS: During a 20-year period, 1941 consecutive patients with renal stone disease underwent routine laboratory procedures including a fasting blood sample for chemistry profile and a 24-hour urine collection for analyses of electrolytes. Thorough histories including chronic inflammatory disease or ileal resection were obtained. Patients with inflammatory bowel disease together with a control group comprising 47 idiopathic renal calcium stone formers were submitted to a xylose absorption test for evaluation of intestinal absorption. RESULTS: We observed 10 patients with Crohn's disease, 12 with ulcerative colitis and one patient with ileal bypass for obesity. Six patients underwent ileal resection and 10 patients total colectomy. Urinary oxalate excretion was significantly higher and urinary citrate lower in stone patients with ileal disease (Ox 60 +/- 23, Cit 113 + 7-118 mg/day) than in idiopathic stone formers (Ox 28.2 +/- 11.5, Cit 381 +/- 205) and stone patients with ulcerative colitis (Ox 20.3 +/- 14.8, Cit 369 +/- 247). Urinary volume was significantly lower in patients with ulcerative colitis. A significant inverse correlation (-0.38, p < 0.01) between oxalate urinary excretion and blood xylose level was found 2 hours after ingestion of xylose. No significant reduction of xylose absorption was demonstrated in both normoxaluric and hyperoxaluric idiopathic stone patients. CONCLUSIONS: Crohn's disease and ulcerative colitis are characterized by recurrent inflammatory involvement of different intestinal segments involving distinctive urinary patterns. Malabosorption associated with ileal disease causes increased oxalate absorption by increasing oxalate solubility in the intestinal lumen and permeability of the colonic mucosa; a reduced citrate excretion is associated in relation to mild acidosis due to the loss of bicarbonate in the liquid stool. In ulcerative colitis, especially if an ileostomy is present, urine are scanty and concentrated, and urine pH falls, leading to uric acid or mixed stones. Mild hyperoxaluria of idiopathic renal stone formers is not related to subtle intestinal malabsorption..
[Note from web owner]
[There are 2 types of high oxalate syndromes: one belonging to those who have a digestive disorder such as IBD and the other being idiopathic renal stone formation. Since autistic children have been found to have a form of intestinal damage that is similar to Crohn's and colitis,most of them will have situation is related to those who have IBD.]
PMID: 12161938 [PubMed - indexed for MEDLINE].
1: Endocrinol Metab Clin North Am. 2002 Dec;31(4):979-99.
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.
PMID: 12474641 [PubMed - indexed for MEDLINE]
More studies that support this hypothesis
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.
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