A 33-year-old man with a 2-year history of Crohn ileocolitis comes to the clinic with left-sided flank pain that started in the morning. The pain is 8 on a scale of 0-10 in intensity and is characterized as sharp. The pain is also colicky and radiates to the left groin. The patient has no nausea or vomiting. He is in moderate distress and has trouble lying still during the examination. Urinalysis shows hematuria. A day later, the patient passes a urinary stone. Abdominal imaging reveals several additional kidney stones. Which of the following is the most likely underlying cause of this patient's kidney stones?
Show Explanatory Sources
Crohn disease is an inflammatory bowel disease characterized by patchy granulomatous inflammation. Any area of the gastrointestinal tract may be involved, but involvement of the terminal ileum is especially common. Bile acids, which facilitate the absorption of fats and fat-soluble vitamins, are normally reabsorbed in the ileum, recycled in the liver, and then reused in the absorptive process. When the terminal ileum is inflamed, bile acids are lost in the feces, leading to impaired fat absorption.
In the healthy bowel, dietary calcium binds to dietary oxalate, producing insoluble calcium oxalate salts that are eliminated in the feces. But in malabsorptive syndromes such as Crohn disease, calcium forms soap complexes with the excess fat in the intestinal lumen and is unavailable for complexing with oxalate. As a result, free oxalate absorption is increased and subsequently filtered into the urine, promoting the formation of oxalate kidney stones (enteric oxaluria).
(Choice A) Cystinuria is an autosomal recessive condition characterized by defective dibasic amino acid transport in the proximal renal tubules. The urine becomes supersaturated with cystine, leading to formation of cystine stones beginning in childhood or adolescence. Crohn disease can cause malabsorption of dietary protein and amino acids, but this is due to inflammation, not abnormal amino acid transporters; patients are not predisposed to cystine stones.
(Choice B) Patients with Crohn disease commonly develop vitamin/nutrient deficiencies (eg, vitamin D, calcium) due to malabsorption, which can reduce bone mineral density and increase the risk of fractures. Secondary hyperparathyroidism may be present, but unlike primary hyperparathyroidism does not promote kidney stone formation.
(Choice C) Uric acid stones may develop from conditions associated with rapid cell turnover (eg, myeloproliferative disease, hemolytic anemia) due to chronically increased uric acid production. The stones seen in Crohn disease are composed of calcium oxalate rather than uric acid.
(Choice E) Alkalinization of the urine by urease-producing organisms (eg, Proteus, Klebsiella) in the upper urinary tract can promote formation of stones made up of magnesium ammonium phosphate (struvite) and calcium carbonate apatite. Although patients with Crohn disease can develop enterovesicular fistulas and recurrent urinary tract infections, this patient has no features of urinary infection (eg, fever, dysuria, pyuria).
Educational objective:
Crohn disease is associated with oxalate kidney stones. Impaired bile acid absorption in the terminal ileum leads to loss of bile acids in feces with subsequent fat malabsorption. Intestinal lipids then bind calcium ions, and the resulting soap complex is excreted. Free oxalate (normally bound by calcium to form an unabsorbable complex) is absorbed and forms urinary calculi (enteric oxaluria).