Between 10 and 15% of adults within the United States will be diagnosed with a kidney stone.
Recurrence rates are estimated at about 10% per year, totaling 50% over a 5–10 year period and 75% over 20 years. Men are affected approximately 4 times more often than women. Recent evidence has shown an increase in pediatric cases. The total cost for treating this condition was $2 billion in 2003.1
Kidney stones are an atypical symptom and associated disorder of celiac disease, however not all people with celiac disease will develop kidney stones. This article describes the pathway for the development of kidney stones that are seen in persons with celiac disease as well as the treatment and prevention.
What is a Kidney Stone?
Kidney stones are deposits of materials, crystallized from urine, that attach to walls of the kidney. One kidney stone is called a renal calculus. Two or more kidney stones are called renal calculi.
80% of kidney stones are formed from calcium oxalate1 and this is the form most often found in celiac disease. Calcium oxalate is the combination of calcium and oxalate. Calcium is an important mineral that the body needs for structure and function. Oxalate is found in foods in the form of oxalic acid. Oxalic acid is an extremely strong acid found in many plant foods. Fortunately, only 8 have been shown to increase urinary oxalate excretion: rhubarb, spinach, strawberries, chocolate, wheat bran, nuts, beets, and tea.2
How Do Kidney Stones Develop?
Kidney stones form when fluid and various minerals and acids in urine are out of balance. When this happens, urine contains more crystal-forming substances than it can hold in solution and crystals precipitate out to form kidney stones that either pass through the urinary tract or become lodged in the kidney or another place along the urinary tract.
Calcium naturally binds with oxalate. In healthy individuals, dietary calcium combines with oxalate in the intestine to form a compound that is not absorbed but is rather eliminated in the stool.
In active celiac disease, the normal mechanism to get rid of oxalate (calcium binding with oxalate) is prevented by fat malabsorption.
If too many fatty acids are present in the intestine, the calcium binds with them instead and is excreted as waste. The oxalate remains to be absorbed into the bloodstream by the colon where it is then excreted into the urine. This process is called enteric hyperoxaluria. “Enteric” means intestinal. “Hyper” means high. “Oxaluria” means oxalate in the urine. Calcium present in the urine binds with the oxalate to form crystals.
In enteric hyperoxaluria, the excess free fatty acids, from fat malabsorption, compete with oxalate for calcium binding, leading to an increased availability of oxalate for absorption (solubility theory). This oxalate is absorbed in the colon, which is made more permeable to unabsorbed bile salts and fatty acids (permeability theory).3
Oxalate that should have combined with calcium in the gut to be properly excreted in stool now shows up in the kidneys where it combines with calcium to be excreted in the urine. Stones form when the amounts of oxalate and calcium are high, the urine is concentrated and the pH (acidity) is low, all of which allow the calcium and oxalate to precipitate out of the urine to remain in the kidney. To illustrate this problem of concentration, think of stirring sugar into a pitcher of lemonade...add too much sugar and it begins to fall to the bottom of the pitcher.
If nothing changes, stones remain in the kidneys to grow and block the passageways of urine excretion.
Oxalobacter Formigenes: The Oxalate Eater. Another cause of high oxalate levels is due to missing bacteria called oxalobacter formigenes. Oxalobacter formigenes is a bacterium (probiotic) found in the gut of most animals. Almost all 6 to 8 year olds have oxalobacter formigenes in their intestines, but only 60 to 80% of adults. Oxalobacter formigenes degrades oxalate by eating it. In fact, oxalate is its only source of food. Unfortunately, it has been shown that oxalobacter formigenes is frequently decreased or missing in people with inflammatory bowel diseases such as celiac disease.4
Treatment & Prevention
The identification and correction of hyperoxaluria is important to prevent recurrent calculi and oxalate nephrosis, especially as patients with kidney stones are often advised to eat a low-calcium diet. Paradoxically, this promotes oxaluria, increasing the risk of further kidney stones in hyperoxaluric patients.3
In most cases, kidney stones will be small enough to pass out of the body by themselves. This can take up to 4 weeks. If the stones are too large, or become lodged along the urinary tract, surgery or Extracorporeal shock wave lithotripsy (ESWL) may be required for removal. ESWL passes electric waves through the body to break up the stones. This is the most common method of removal.
The general treatment is maintenance of high urine output through oral hydration and avoidance of dietary excess.5
Optimal treatment for people with celiac disease involves a 100% strict gluten-free diet, correcting fat malabsorption, increasing calcium intake, increasing fluid intake, decreasing oxalate absorption and protecting colonies of the intestinal probiotic, oxalobacter formigenes. Future therapies may include oxalobacter formigenes supplementation.
100% Strict Gluten-Free Diet. This is self-explanatory. Even 1 mg of gliadin per day can cause intestinal damage in some people, so zero tolerance should be the goal.
Increasing Calcium Intake. Calcium combines with oxalate, so increasing calcium ingestion will remove more oxalate in the intestine. It is important to note that any recommended treatment for kidney stones that limits or restricts calcium in the diet will make them worse in a person with celiac disease. Calcium restriction has been shown to have no effect on kidney stone formation. If calcium is restricted, kidney stones will still form, the parathyroid will become overtaxed and osteoporosis will accelerate. This is because in patients with untreated celiac disease, calcium is not absorbed but calcium levels must be maintained in the blood. The parathyroid acts to pull calcium from the bones to maintain this level.
Increasing Fluid Intake. Enough water must be ingested to produce 2 to 2.5 liters of urine per day. Sources of urine concentration must be corrected. Diarrhea is one cause of concentrated urine because fluid is lost in the stool. Bicarbonate is also lost by diarrhea, which then lowers the pH, making the body more acidic. Diarrhea must be corrected if present. Thiamin deficiency will decrease thirst. Thiamin deficiency must be corrected.
Decreasing Oxalate. Only eight foods have been proven to increase urinary oxalate excretion. Those foods are rhubarb, spinach, strawberries, chocolate, wheat bran, nuts, beets and tea.2 These foods should be avoided. Of course, wheat bran should never be consumed by anyone with celiac disease with or without kidney stones. If the foods are ingested, combining them with calcium rich foods will limit oxalate absorption.
Protecting Oxalobacter Formigenes Colonies. Research has demonstrated that supplementing oxalobacter formigenes reduces oxalate levels in the urine. Oxalobacter formigenes deficiency can be caused by certain antibiotics, low pH levels in the intestine and possibly other factors as yet unknown. Antibiotics that kill oxalobacter formigenes include clarithromycin (Klaracid), doxycycline (Vibramycin), chloramphenicol, erythromycin, amoxicillin plus clavulanic acid.4
Prognosis is good in those who strictly follow the gluten-free diet, correct fat malabsorption and absorb sufficient calcium. When fat in the diet is properly absorbed in the small intestine, calcium should properly bind oxalate, thereby correcting the cause of kidney stone formation. If celiac disease remains untreated, the alternative is progression of stones that damage the kidney and interfere with its work of cleansing the blood.
A case report of a 49 year old man with renal colic and left renal calculus describes celiac disease presenting with kidney stones in the absence of gastrointestinal symptoms. The presence of hyperoxaluria with hypercalciuria prompted malabsorption studies with discovered celiac disease. 3 months on a gluten free diet led to normalization of urinary oxalate excretion.3
Another case report describes a 10 year old girl with fat malabsorption hyperoxaluria and kidney stones in a single functioning kidney presenting with celiac disease. Successful management of the fat malabsorption in the gluten-free diet corrected the hyperoxaluria. Pediatricians caring for children presenting with kidney stones or hyperoxaluria should investigate them for celiac disease.3
Kidney stones can damage or even destroy the kidney. This article demonstrates the seriousness of celiac disease. Repercussions from not following a strict gluten-free diet can be severe or deadly. If you or someone you know has a problem with kidney stones that has not resolved under normal treatment, celiac disease may be the underlying cause.
- Wikipedia. http://en.wikipedia.org/wiki/Kidney_stone
- Kathleen Mahan and Sylvia Escott-Stump, ed. Krause’s Food, Nutrition, & Diet Therapy, 10th Edition. Philadelphia, PA, USA: W.B. Saunders Company, 2000.
- Cleo J. Libonati. Recognizing Celiac Disease, Fort Washington, PA, USA: GFW Publishing, 2007. www.recognizingceliacdisease.com
- Duncan SH, Richardson AJ, Kaul P, et al. Oxalobacter formigenes and its potential role in human health. Applied and Environmental Microbiology, Aug 2002: 3841-3847.
- The Washington Manual of Medical Therapeutics, 30th Edition, Lippincott Williams & Wilkins, 2001. p. 274.