Patients who undergo gastric bypass procedures develop changes in their urinary chemistry that increase their risk for developing nephrolithiasis. Patients who undergo the most common type of gastric bypass surgery, the Roux-en-Y (RYGB), whereby creation of a small gastric pouch so food bypasses part of the small intestines, are at increased risk for calcium oxalate kidney stones beginning 6 months after surgery. In one study, the risk of stones was 7.65 % compared to 4.63 % in the control group [12]. The added kidney stone risk is thought to be due to changes in the urinary chemistry. Patients who have undergone Roux-en-Y gastric bypass surgery have excess oxalate and low levels of citrate in their urine after the procedure.

Other types of weight loss surgery, including gastric banding, is not associated with an increased risk for kidney stones or kidney stone surgeries [13].

Recommendations to reduce an individual’s risk for stones following gastric bypass is to increase fluid intake, limit oxalate containing foods, reduce sodium intake and red meat consumption.

Short bowel syndrome, is a condition that generally occurs when portions of the small intestines are surgically removed. It causes an inability to properly absorb fat and nutrients. These patients may develop steatorrhea, a condition whereby there is excess fat in the stool. Calcium may bind to the unabsorbed fatty acids, resulting in a condition referred to as saponification. This allows increased concentration of free oxalate in the bowl lumen to be absorbed in the colon resulting in hyperoxaluria. As a result of low urine volume, Hypocitraturia, hypomagnesuria and hyperoxaluria, these patients are at an increased risk of developing calcium oxalate stones. Prevention of stones involves a low fat, low oxalate diet, increased fluid consumption to increase urine volume, oral calcium to bind oxalate in the gut lumen and citrate and magnesium replacement [14].

Patients with an ileostomy and individuals with a colon resection have a tendency to chronic volume contraction due to loss of water, bicarbonate and potassium in diarrheal stool, leading to reduced urine volumes. These individuals also have decreased absorption of citrate and magnesium, resulting in less inhibitory action on calcium oxalate crystallization. As a result, these patients have a tendency to produce calcium oxalate stones. These patients also form uric acid stones as a result of bicarbonate loss in the ileostomy resulting in acidic urine combined with watery stools and low urine volume. Therapy is directed by alkalization of the urine to a pH of 6.5, increasing urine volume to increase the solubility of uric acid to prevent crystallization [14]. These stones are often very difficult to prevent without decreases in diarrhea/ileostomy losses.

Nephrolithiasis may be produced by a number of prescription and nonprescription drugs used to treat a variety of medical conditions. These drugs may lead to metabolic abnormalities that initiate the formation of urinary tract stones. Approximately 1–2 % of renal calculi are drug-induced. Drugs that induce metabolic calculi include diuretics, carbonic anhydrase inhibitors, and abuse of laxatives. Correcting the underlying metabolic abnormality may reverse or eliminate the stone formation process.

Urinary calculi can also be produced by medications when the drugs crystallize (i.e., urinary supersaturation) and become the primary component of the stone. Medications that initiate this process include magnesium trisilicate, Ciprofloxacin, sulfa medications, triamterene, indinavir, and ephedrine with or without guaifenesin. When this situation occurs, cessation of the medication is usually necessary to reverse this process.