A 35-year-old man comes to the emergency department due to acute-onset left-sided flank pain, hematuria, and vomiting. He has regular bowel movements. Medical history is significant for Crohn disease complicated by multiple strictures that required surgical resection of the small intestine. Temperature is 36.8 C (98.2 F), blood pressure is 120/65 mm Hg, pulse is 110/min, and respirations are 16/min. BMI is 22 kg/m2. The abdomen is soft and mildly tender over the left flank with no rebound or rigidity. Bowel sounds are decreased. A laparotomy scar is present. Which of the following is the most likely cause of this patient's symptoms?
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This patient has flank pain, hematuria, and vomiting suggestive of nephrolithiasis. Given his history of Crohn disease and small bowel resection, he likely has fat malabsorption that has predisposed him to hyperoxaluria and calcium oxalate stones.
Under normal conditions, dietary calcium binds dietary oxalate in the intestine, forming insoluble calcium oxalate salts that are eliminated in the feces. In malabsorption syndromes that develop with small bowel disease (eg, Crohn disease) or surgical small bowel diversion (eg, gastric bypass), excess fatty acids (which are normally reabsorbed in the ileum) remain in the intestinal lumen. These fatty acids form complexes with calcium and decrease the amount of calcium available for binding oxalate. As a result, enteric oxalate absorption is increased. Oxalate is subsequently filtered into the urine, where an increased level (ie, hyperoxaluria) promotes the formation of calcium oxalate stones.
(Choice A) Increased enteric absorption of calcium, induced by calcitriol (the active form of vitamin D), results in hypercalcemia, hypercalciuria, and an increased risk of calcium stones. Conditions that increase calcitriol levels include hyperparathyroidism (via increased renal hydroxylation of calcidiol) and granulomatous diseases like sarcoidosis (via extrarenal production of calcitriol by macrophages). There is nothing in this patient's clinical history to suggest either disorder; his history of Crohn disease makes hyperoxaluria the more likely cause of nephrolithiasis.
(Choice C) Increased recycling of bile salts and fatty acids would reduce the amount available to bind dietary calcium. This would result in more calcium available to bind dietary oxalate, which would limit enteric oxalate absorption, reduce the concentration of urinary oxalate, and decrease the risk for calcium oxalate stones. Malabsorption syndromes (eg, Crohn disease, small bowel resection) decrease (not increase) recycling of bile salts and fatty acids.
(Choice D) Increased urinary citrate excretion would be protective against nephrolithiasis. Citrate inhibits the formation of calcium stones by binding with urinary calcium and creating a complex that is soluble in urine.
(Choice E) Increased urinary uric acid excretion, seen in gout and myeloproliferative disorders, predisposes patients to uric acid stones. This patient's risk of hyperoxaluria from Crohn disease makes calcium oxalate stones more likely.
Educational objective:
In malabsorption syndromes (eg, Crohn disease), excess luminal fatty acids sequester dietary calcium, which reduces calcium binding of oxalate and allows more oxalate to be enterically absorbed. Oxalate is subsequently filtered into the urine, where an increased level (ie, hyperoxaluria) promotes calcium oxalate stone formation.