Malabsorptive Disorders and Inflammatory Bowel Disease: Assessing and Improving Nutritional Stone Risk

The relationship between calcium oxalate kidney stone formation and inflammatory bowel disease (IBD) was first noted in two large retrospective case series from the 1960s. In over 1,400 patients with inflammatory bowel disease, 92 of 1,468 patients (6%) were identified to have developed renal stones, an occurrence that appeared as frequent as other systemic complications of this disease process [1, 2]. The mechanisms behind this high stone incidence were confirmed in the 1970s to be a complication of fat malabsorption and chronic diarrhea, which resulted in enteric hyperoxaluria, decreased urine citrate concentration and pH, and decreased urine volumes [3, 4]. Since those early descriptions, other malabsorptive intestinal disease states have also been added to the IBD/stone- associated list, including jejunoileal bypass (historical) and Roux-en-Y gastric bypass for obesity, chronic mesenteric ischemia, and small bowel ostomies [5, 6]. In general, patients with ileocolonic disease (9–17%) tend to be more commonly affected than those with ileal (6–8%) or colonic disease (3–5%) alone, and stone composition varies between calcium oxalate (malabsorptive diseases, ileocolonic Crohn’s disease) and uric acid (copious diarrhea, small bowel ostomies) depending on the disease state and amount of volume loss/diarrhea. This chapter will highlight the urinary abnormalities seen in modern bariatric surgical patients and in patients with the two most common forms of IBD (Crohn’s, ulcerative colitis) with a focus on the nutritional aspects that can be improved in these stone-forming populations.