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.