In addition to hyperoxaluria, RYGB patients develop hypocitraturia secondary to GI fluid losses, further increasing the risk of calcium oxalate supersaturation and stone formation. Based on both clinical and experimental data, a portion of RYGB patients have been shown to acquire metabolic acidosis after RYGB [11], believed to be due to gut bicarbonate and fluid losses secondary to chronic diarrhea. This acidosis leads to increased mitochondrial citrate utilization, renal citrate reabsorption, and decreased urinary citrate secretion. Citrate, a natural inhibitor of calcium crystallization, complexes with urinary calcium to lower calcium crystal saturation while raising urine pH. Therefore, RYGB patients with hypocitraturia are at further increased risk of calcium stone formation due to lowered urine pH and altered supersaturation. Finally , the restrictive component of RYGB may lower the amount of fluids these patients can ingest. This, combined with GI volume loss from chronic diarrhea, lowers the volume of urine production and increases urinary crystal supersaturation risk.

Kidney stone formation , particularly calcium oxalate stones, in RYGB patients is a complex interplay of various environmental and nutritional components. With these mechanisms, there are several recommendations one can provide to patients to minimize stone formation. Many of these strategies are similar to those recommended to all stone formers and are summarized in Table 15.2. These include increasing daily fluid intake to achieve urine volumes of >2 l/day and low oxalate intake of <100 mg/day. Additionally, low sodium and animal protein intake, as seen in the Dietary Approaches to Stop Hypertension (DASH) diet , may encourage favorable dietary patterns and impart a more balanced approach rather than one of “food avoidance.” This is particularly important when counseling patients as sodium and animal-based protein are prevalent in the American diet. As discussed earlier, fatty acids result in increased elimination of intestinal calcium and therefore more free oxalate. As such, RYGB patients can simply reduce their daily fat intake as well as increase calcium intake in the form of calcium citrate. Calcium citrate is preferred over calcium carbonate as it also aids in correcting metabolic acidosis and hypocitraturia, further decreasing the risk of stone formation [12, 13]. Other options for these patients include supplementation with probiotics and pyridoxine. Although the data in this area is limited, a brief review of these nutritional factors is important.

Oxalobacter formigenes is an anaerobic gut commensal bacterium that uses oxalate as its sole energy source. Because higher free gut luminal oxalate may lead to enhanced oxalate absorption and stone disease, lack of Oxalobacter colonization in calcium oxalate stone formers has been linked as a potential etiology of hyperoxaluria [14]. In 2005, patients with fat malabsorption, hyperoxaluria, and calcium oxalate stones caused by a variety of GI diseases, including six patients RYGB patients, were given the probiotic “Oxadrop®” (Lactobacillus acidophilus and brevis, Streptococcus, and Bifidobacterium) [15]. Over a period of 3 months, mean urinary oxalate levels decreased by 20% in these patients with fairly resistant hyperoxaluria [15]. This trial was followed by several encouraging case series in primary hyperoxaluria (PH) patients, a rare genetic disease characterized by abnormally high hepatic oxalate synthesis and high urinary oxalate excretion. These series showed reductions in urinary oxalate excretion in PH patients administered with viable Oxalobacter cells [16]. However, a recent multicenter randomized trial of orally administered O. formigenes in PH patients showed no difference in urinary oxalate levels between the treatment and control group [17]. Due to these discrepancies, Canales et al. evaluated the efficacy of orally administered O. formigenes in a rat model of RYGB surgery and found that urinary oxalate fell more than 70% over an 8-week bacterial gavage course [9]. Although more clinical trials are needed in this population, it seems reasonable to suggest that RYGB-stone formers try probiotics in the form of yogurt if they experience hyperoxaluria, as yogurt contains calcium (an oxalate binder) as well as forms of probiotics that may have beneficial effects on gut oxalate handling.

Pyridoxal L-phosphate (PLP ) , the metabolically active form of vitamin B6, is an important cofactor for the transamination reaction of glyoxylate to glycine. In the setting of vitamin B6 deficiency, the pathway is shunted from glycine production to that of oxalate, resulting in excessive urinary oxalate [18]. Vitamin B6 is water soluble and is not typically deficient in the American diet. However, a retrospective series of over 400 gastric bypass patients demonstrated that almost 20% of these patients were vitamin B6 deficient at 1 and 2 years postsurgery [19]. Although these patients did not have corresponding urine oxalate levels to determine causality, it seems reasonable to presume that B6 deficiency could lead to increased liver oxalogenesis, hyperoxaluria , and calcium oxalate stone disease (Fig. 15.1). More studies are needed in this area, especially because a retrospective study of empiric vitamin B6 supplementation in addition to dietary counseling in patients with idiopathic hyperoxaluria noted an approximately 30% decrease in urine oxalate on follow-up 24-h urine studies [20]. Lastly, due to light sensitivity, serum PLP can be difficult to measure accurately, and many clinical labs do not offer this as quantitative study. Because of this, many practitioners offer low-dose supplementation in lieu of measuring PLP levels. Vitamin B6 can cause neurotoxicity at high levels, so a reasonable supplement regimen is around 50 mg daily for 6 months with discontinuation of the supplement after that time period (Table 15.2).