Abstract: The current obesity epidemic in the United States has deleterious effects on the health of the population. Temporally related to the increase in obesity is an increase in the prevalence of urolithiasis. Epidemiologic studies have shown that the incident stone risk increases with body mass index. Obesity can increase stone risk in multiple ways. Excess nutritional intake increases traffic of lithogenic substances such as calcium, oxalate, and uric acid. Metabolic syndrome, commonly associated with obesity, alters renal acid-base metabolism, resulting in a lower urine pH and increased risk of uric acid stone disease. The low urine pH is caused by deficient ammonia production, which appears to be related to insulin resistance. Even weight-loss programs to combat obesity can influence stone risk. Contemporary bariatric surgery has been shown to frequently cause hyperoxaluria with associated stone formation and even oxalate nephropathy. Commonly used low-carbohydrate diets increase the risk of both calcium and uric acid stones. Certainly, the many health risks of obesity, including urolithiasis, necessitate weight loss, but recognition of the potential complications of such therapies is required to prevent induction of new and equally severe medical problems. The optimal approach to weight control that minimizes stone risk needs to be determined. The current obesity epidemic in the United States has deleterious effects on the health of the population. Temporally related to the increase in obesity is an increase in the prevalence of urolithiasis. Epidemiologic studies have shown that the incident stone risk increases with body mass index. Obesity can increase stone risk in multiple ways. Excess nutritional intake increases traffic of lithogenic substances such as calcium, oxalate, and uric acid. Metabolic syndrome, commonly associated with obesity, alters renal acid-base metabolism, resulting in a lower urine pH and increased risk of uric acid stone disease. The low urine pH is caused by deficient ammonia production, which appears to be related to insulin resistance. Even weight-loss programs to combat obesity can influence stone risk. Contemporary bariatric surgery has been shown to frequently cause hyperoxaluria with associated stone formation and even oxalate nephropathy. Commonly used low-carbohydrate diets increase the risk of both calcium and uric acid stones. Certainly, the many health risks of obesity, including urolithiasis, necessitate weight loss, but recognition of the potential complications of such therapies is required to prevent induction of new and equally severe medical problems. The optimal approach to weight control that minimizes stone risk needs to be determined. Kidney stones are caused by both genetic and environmental influences. Twin studies suggest that approximately 50% of stone risk is genetic in origin; the remainder of stone risk is because of a combination of diet, exercise, work environment, and geography.1Goldfarb D.S. Fischer M.E. Keich Y. et al.A twin study of genetic and dietary influences on nephrolithiasis: a report from the Vietnam Era Twin (VET) Registry.Kidney Int. 2005; 67: 1053-1061Crossref PubMed Scopus (198) Google Scholar Multiple studies from industrialized countries have shown that the prevalence of kidney stone disease is increasing.2Trinchieri A. Coppi F. Montanari E. et al.Increase in the prevalence of symptomatic upper urinary tract stones during the last ten years.Eur Urol. 2000; 37: 23-25Crossref PubMed Scopus (172) Google Scholar, 3Serio A. Fraioli A. Epidemiology of nephrolithiasis.Nephron. 1999; 81: 26-30Crossref PubMed Scopus (103) Google Scholar, 4Stamatelou K.K. Francis M.E. Jones C.A. et al.Time trends in reported prevalence of kidney stones in the United States: 1976-1994.Kidney Int. 2003; 63: 1817-1823Crossref PubMed Scopus (1142) Google Scholar Stamatelou et al4Stamatelou K.K. Francis M.E. Jones C.A. et al.Time trends in reported prevalence of kidney stones in the United States: 1976-1994.Kidney Int. 2003; 63: 1817-1823Crossref PubMed Scopus (1142) Google Scholar compared data from the US National Health and Nutrition Examination Surveys (NHANES) to show an increase in prevalence of urolithiasis from 3.8% to 5.2% between 1976 and 1994. Certainly, such short-term trends must be related to changes in diet and lifestyle and not a change in the genome. Over a similar time frame, the United States has been in the midst of an obesity epidemic.5Archenti A. Pasqualinotto L. Childhood obesity: The epidemic of the third millenium.Acta Biomed. 2008; 79: 151-155PubMed Google Scholar, 6Wang Y. Beydoun M.A. Liang L. et al.Will all Americans become overweight or obese? Estimating the progression and cost of the US obesity epidemic.Obesity. 2008; 16: 2323-2330Crossref PubMed Scopus (1071) Google Scholar In this article, the relationship of obesity to stone formation is explored, from issues related to overconsumption of food, the metabolic effects of obesity itself, and the potential risk of weight-reduction programs on stone risk. In the last 20 years, the United States suffered epidemic levels of obesity. Data from NHANES studies showed in 2004 that 32% of adults were obese and 17% of children and adolescents were overweight.7Ogden C.L. Carroll M.D. Curtin L.R. et al.Prevalence of overweight and obesity in the United States, 1999-2004.JAMA. 2006; 295: 1549-1555Crossref PubMed Scopus (7390) Google Scholar Even between 1999 and 2004, the NHANES III survey detected a significant increase in the prevalence of overweight children, indicating that the obesity epidemic had continued to spread, despite widespread documentation of this problem in the lay press. There were multiple causes of the obesity epidemic including, but not limited to, larger portions of food, increased fructose consumption, more sedentary lifestyle, a decrease in tobacco use, and reduced levels of physical labor.6Wang Y. Beydoun M.A. Liang L. et al.Will all Americans become overweight or obese? Estimating the progression and cost of the US obesity epidemic.Obesity. 2008; 16: 2323-2330Crossref PubMed Scopus (1071) Google Scholar, 8Roth J. Qiang X. Marban S.L. et al.The obesity pandemic: where have we been and where are we going?.Obes Res. 2004; 12: 88S-101SCrossref PubMed Scopus (191) Google Scholar, 9Nielsen S.J. Popkin B.M. Patterns and trends in food portion sizes, 1977-1998.JAMA. 2003; 289: 450-453Crossref PubMed Scopus (796) Google Scholar A comparison of NHANES studies from 1962 through the 2000 survey showed that the prevalence of obesity was approximately 15% in the adult population from 1962 to 1980 and grew thereafter (Fig 1). This growth correlated with an increase in prevalence of stone disease.10Flegal K.M. Carroll M.D. Ogden C.L. et al.Prevalence and trends in obesity among US adults, 1999-2000.JAMA. 2002; 288: 1723-1727Crossref PubMed Scopus (5355) Google Scholar However, correlation does not prove causality. In 2005, Taylor et al11Taylor E.N. Stampfer M.J. Curhan G.C. Obesity, weight gain, and the risk of kidney stones.JAMA. 2005; 293: 455-462Crossref PubMed Scopus (845) Google Scholar studied the association of obesity and weight gain with the risk of forming an incident kidney stone in 3 large cohorts followed prospectively for a total of 46 years. As shown in Figure 2, as body mass index (BMI) increased, the risk of stone formation increased significantly in all 3 cohorts, even after adjusting for age and dietary factors. The increase in relative risk with BMI was greater for the 2 female cohorts from the Nurses' Health Study I and II (NHS I and II) than the male cohort of the Health Professionals Follow-up Study (HPFS). In addition, weight gain since early adulthood was shown to increase risk in all 3 cohorts, supporting the premise that the excess stone risk is caused by greater adiposity because weight gain after early adulthood is usually from a gain of fat and not lean body mass. Unfortunately, the epidemiologic evidence of a link between obesity and urolithiasis does not provide a mechanism for stone formation. In assessing the relationship of obesity and urolithiasis, consideration must be given to how dietary intake impacts urine lithogenicity as well as how alterations in metabolism are directly related to obesity itself. In 2000, Powell et al12Powell C.R. Stoller M.L. Schwartz B.F. et al.Impact of body weight on urinary electrolytes in urinary stone formers.Urology. 2000; 55: 825-830Abstract Full Text Full Text PDF PubMed Scopus (179) Google Scholar performed one of the first studies to address the effect of obesity on urine stone risk factors. Using data from 5,942 stone-forming patients from a national kidney stone laboratory, they compared 24-hour urine chemistries of obese patients (definition: males >120 kg and females >100 kg) with nonobese patients. They found the obese stone formers had higher excretion rates of calcium, oxalate, and uric acid accompanied by a lower urine pH, all of which increase kidney stone risk. Offsetting these stone risk factors was a higher urine citrate and urine volume. They also found that urine sodium and sulfate were higher in the obese subjects. Because the excretion of sodium and sulfate is directly related to the intake of salt and protein, respectively, their findings suggest that at least some of the risk for stone formation in obesity comes from excessive food intake. Siener et al13Siener R. Glatz S. Nicolay C. et al.The role of overweight and obesity in calcium oxalate stone formation.Obes Res. 2004; 12: 106-113Crossref PubMed Scopus (221) Google Scholar published a similar study of urine chemistries from 527 idiopathic calcium oxalate stone formers. By linear regression analysis, the authors determined significant positive correlations in both sexes between BMI and uric acid and sodium and phosphorus excretion. A negative correlation existed between BMI and urine pH in both sexes. There was also a correlation between BMI and calcium only in men and oxalate and BMI only in women. Unlike the study by Powell et al, there was not an increase in citrate or urine flow rate with increasing BMI. Both of these studies were performed in patients with urolithiasis so the association of stone risk and obesity could not be applied to the non–stone-forming population. Subsequently, Taylor and Curhan14Taylor E.N. Curhan G.C. Body size and 24-hour urine composition.Am J Kidney Dis. 2006; 48: 905-915Abstract Full Text Full Text PDF PubMed Scopus (240) Google Scholar performed 24-hour urine studies on subsets of 3 large cohort studies (NHS I and II and HPFS), including subjects with and without a history of kidney stone disease. Using linear regression adjusted for kidney stone history, dietary intake, and other urine chemistries, they found subjects with higher BMIs had higher urine excretion rates of oxalate, sodium, uric acid, and phosphorus as well as a lower urine pH. Calcium, which had been positively correlated with BMI in the male and young female cohorts, did not correlate with BMI after adjustment for urine sodium and phosphorous excretion. This lack of association between BMI and adjusted urine calcium excretion suggests the higher calcium excretion in obese subjects may not be related to underlying changes in physiology from obesity but is instead heavily influenced by the composition of the diet. In addition to increased caloric intake in general, consumption of specific foodstuffs may impart specific risk for stone formation. Fructose has drawn much interest in relation to the obesity epidemic. Temporally, the widespread addition of high-fructose corn syrup to the American diet, which began in 1967, has correlated with the increase of obesity and metabolic syndrome.15Gross L.S. Li L. Ford E.S. et al.Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: An ecologic assessment.Am J Clin Nutr. 2004; 79: 774-779PubMed Scopus (501) Google Scholar Fructose may even stimulate weight gain beyond the effects on caloric intake by directly inducing leptin resistance and thus preventing the feeding inhibitory effects of leptin.16Shapiro A. Mu W. Roncal C.A. et al.Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high fat feeding.Am J Physiol Regul Integr Comp Physiol. 2008; 295: R1370-R1375Crossref PubMed Scopus (228) Google Scholar Fructose consumption has been reported to have many potential effects that could directly increase stone risk beyond the risk conferred by weight gain and metabolic syndrome. Fructose has been shown to increase urine calcium excretion when fed to rats and in limited studies in humans.17Koh E.T. Reiser S. Fields M. Dietary fructose as compared to glucose and starch increases the calcium content of kidney of magnesium-deficient rats.J Nutr. 1989; 119: 1173-1178PubMed Scopus (24) Google Scholar, 18Milne D.B. Nielsen F.H. The interaction between dietary fructose and magnesium adversely affects macromineral homeostasis in men.J Am Coll Nutr. 2000; 19: 31-37Crossref PubMed Scopus (52) Google Scholar Fructose also increases uric acid production and urinary excretion in humans, increasing the risk of both uric acid and calcium oxalate stone formation.19Fox I.H. Kelley W.N. Studies on the mechanism of fructose-induced hyperuricemia in man.Metabolism. 1972; 21: 713-721Abstract Full Text PDF PubMed Scopus (158) Google Scholar Using data from the NHS (I and II) and the HPFS studies, Taylor and Curhan20Taylor E.N. Curhan G.C. Fructose consumption and the risk of kidney stones.Kidney Int. 2008; 73: 207-212Crossref PubMed Scopus (160) Google Scholar have shown that increasing fructose intake was associated with a higher relative risk of forming incident kidney stones (Fig 3) even after adjusting for BMI, caloric intake, and other dietary factors. By separating the effects of caloric intake and weight, these data support the premise that fructose ingestion by itself may increase stone risk in addition to potential risk imposed by the obesity often associated with the overconsumption of high-calorie foods. Metabolic syndrome is a constellation of clinical and laboratory findings that identifies people with an increased risk of cardiovascular disease.21Pi-Sunyer X: The metabolic syndrome: how to approach differing definitions.Med Clin North Am. 2007; 91: 1025-1040Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar Included in the diagnostic criteria are glucose intolerance, increased abdominal girth, hypertension, and dyslipidemia, all of which would be expected to be found at a high rate in an obese population. As the prevalence of obesity has increased, so has the prevalence of metabolic syndrome and type 2 diabetes. These temporal associations suggest that there may be a link between diabetes, metabolic syndrome, and stone disease. Recently, there have been a number of studies suggesting that type 2 diabetes mellitus and metabolic syndrome are related to an increased risk of uric acid stone formation. In a retrospective analysis of 3,561 patients with nephrolithiasis with matched controls, Lieske et al22Lieske J.C. de la Vega L.S. Gettman M.T. et al.Diabetes mellitus and the risk of urinary tract stones: A population-based case-control study.Am J Kidney Dis. 2006; 48: 897-904Abstract Full Text Full Text PDF PubMed Scopus (113) Google Scholar found an increased adjusted odds ratio for diabetes among the stone formers (odds ratio = 1.22; 95% confidence interval [CI], 1.03-1.46). Taylor et al,23Taylor E.N. Stampfer M.J. Curhan G.C. Diabetes mellitus and the risk of nephrolithiasis.Kidney Int. 2005; 68: 1230-1235Crossref PubMed Scopus (383) Google Scholar using data from the NHS and HPFS cohort studies, found an increased multivariate relative risk (RR) of stone formation in those subjects who reported having diabetes compared with those without (RR = 1.38; 95% CI, 1.06-1.79 in older females; RR = 1.67; 95% CI, 1.28-2.20 in younger females; and RR = 1.31; 95% CI, 1.11-1.54 in males). However, stone analysis was not available in either of these studies, and it is unclear whether diabetics are at increased risk for all types of kidney stones. Daudon et al24Daudon M. Traxer O. Conort P. et al.Type 2 diabetes increases the risk for uric acid stones.J Am Soc Nephrol. 2006; 17: 2026-2033Crossref PubMed Scopus (244) Google Scholar reported the results of stone analysis in 2,464 patients, of which 272 had diabetes. The proportion of uric acid stones of the diabetic patients was 3 times higher than of the nondiabetics. Although this study implied that there are metabolic derangements that increase the risk of uric acid stone formation in type 2 diabetes, it did not address the rate of stone formation and therefore did not exclude the possibility that the rates of calcium and uric acid stone formation were increased in diabetes and that the risk for uric acid risk stone development may have superseded the calcium stone risk. Uric acid crystallization in humans is dependent on 3 factors: uric acid excretion, urine flow rate, and urine pH.25Asplin J. Uric acid stones.Semin Nephrol. 1996; 16: 412-424PubMed Google Scholar In order for uric acid stones to form in patients with diabetes and/or metabolic syndrome, one or more of these factors must be affected. In the vast majority of patients with uric acid kidney stones, uric acid excretion is normal, whereas urine pH is markedly reduced.26Pak C.Y. Sakhaee K. Peterson R.D. et al.Biochemical profile of idiopathic uric acid nephrolithiasis.Kidney Int. 2001; 60: 757-761Crossref PubMed Scopus (145) Google Scholar Because the pK of uric acid in urine is 5.35, as urine pH falls within its physiologic range, a larger percentage of uric acid is protonated, generating the least soluble form of uric acid.27Coe F.L. Strauss A.L. Tembe V. et al.Uric acid saturation in calcium nephrolithiasis.Kidney Int. 1980; 17: 662-668Crossref PubMed Scopus (78) Google Scholar Because acidic urine is the sine qua non of the uric acid stone former, a number of studies have searched for a link among diabetes, obesity, metabolic syndrome, and urine pH. Data from 2 large kidney stone clinics have documented an inverse correlation between urine pH and body weight.28Maalouf N.M. Sakhaee K. Parks J.H. et al.Association of urinary pH with body weight in nephrolithiasis.Kidney Int. 2004; 65: 1422-1425Crossref PubMed Scopus (330) Google Scholar In addition, type 2 diabetes had lower urine pH values than normal subjects, and this relationship was independent of whether uric acid stones had been formed previously.29Cameron M.A. Maalouf N.M. Adams-Huet B. et al.Urine composition in type 2 diabetes: predisposition to uric acid nephrolithiasis.J Am Soc Nephrol. 2006; 17: 1422-1428Crossref PubMed Scopus (178) Google Scholar Finally, patients with uric acid stones were commonly found to have features of the metabolic syndrome.30Sakhaee K. Adams-Huet B. Moe O.W. et al.Pathophysiologic basis for normouricosuric uric acid nephrolithiasis.Kidney Int. 2002; 62: 971-979Crossref PubMed Scopus (258) Google Scholar To further explore the relationship of low urine pH and metabolic syndrome, Maalouf et al31Maalouf N.M. Cameron M.A. Moe O.W. et al.Low urine pH: A novel feature of the metabolic syndrome.Clin J Am Soc Nephrol. 2007; 2: 883-888Crossref PubMed Scopus (213) Google Scholar collected 24-hour urine specimens from 148 non–stone-forming subjects. They found that subjects with the metabolic syndrome had a significantly lower urine pH than those without it. When subjects were classified by the number of metabolic syndrome criteria present, the urine pH decreased with the presence of each additional metabolic syndrome criterion (Fig 4).31Maalouf N.M. Cameron M.A. Moe O.W. et al.Low urine pH: A novel feature of the metabolic syndrome.Clin J Am Soc Nephrol. 2007; 2: 883-888Crossref PubMed Scopus (213) Google Scholar The pathophysiology of acidic urine in metabolic syndrome is an emerging area of interest. In a comparison of 55 healthy subjects and 13 recurrent uric acid stone formers, the latter showed insulin resistance during hyperinsulinemic, euglycemic clamp studies.32Abate N. Chandalia M. Cabo-Chan Jr., A.V. et al.The metabolic syndrome and uric acid nephrolithiasis: Novel features of renal manifestation of insulin resistance.Kidney Int. 2004; 65: 386-392Crossref PubMed Scopus (441) Google Scholar Even in non–stone-forming subjects, glucose disposal rates correlated with urine pH, supporting the hypothesis that insulin resistance plays a role in the generation of low urine pH, which appears to be caused by 2 separate acid base abnormalities.29Cameron M.A. Maalouf N.M. Adams-Huet B. et al.Urine composition in type 2 diabetes: predisposition to uric acid nephrolithiasis.J Am Soc Nephrol. 2006; 17: 1422-1428Crossref PubMed Scopus (178) Google Scholar, 30Sakhaee K. Adams-Huet B. Moe O.W. et al.Pathophysiologic basis for normouricosuric uric acid nephrolithiasis.Kidney Int. 2002; 62: 971-979Crossref PubMed Scopus (258) Google Scholar, 32Abate N. Chandalia M. Cabo-Chan Jr., A.V. et al.The metabolic syndrome and uric acid nephrolithiasis: Novel features of renal manifestation of insulin resistance.Kidney Int. 2004; 65: 386-392Crossref PubMed Scopus (441) Google Scholar First, there is a relative suppression of ammonia excretion, which increases the proportion of the daily acid load that is excreted as titratable acid. Second, patients with metabolic syndrome and/or type 2 diabetes have a greater net acid excretion than normal subjects even when placed on a fixed diet within a clinical research center. Whether the increased net acid excretion is attributed to lower urine losses of unmeasured alkali or from overproduction of organic acid has not been determined. One question that has not been well studied is whether weight reduction will reverse the metabolic abnormalities associated with uric acid stone formation. In 1 study of 52 subjects with gout, the effect of peroxisome proliferator-activated receptor agonists, which improve insulin sensitivity, was to increase urine pH during treatment without weight loss.33Takahashi S. Inokuchi T. Kobayashi T. et al.Relationship between insulin resistance and low urinary pH in patients with gout, and effects of PPAR alpha agonists on urine pH.Horm Metab Res. 2007; 39: 511-514Crossref PubMed Scopus (32) Google Scholar It seems likely that weight loss, which enhances insulin sensitivity, would increase urine pH, but this remains to be proven. In the 1960s, bariatric surgery was in its infancy. The first procedure to gain widespread acceptance was the jejunoileal bypass (JIB). In JIB, the terminal 10 cm of ileum is connected to the proximal jejunum, bypassing the bulk of the jejunum and proximal ileum, which greatly reduces the available absorptive surface of the intestinal tract. The procedure induced weight loss through malabsorption. Food intake was unlimited, except for patients' concerns for dealing with the diarrhea from malabsorption. Overall patient satisfaction was high because dietary intake was not restricted. However, over time, complications such as liver disease, arthritis, malnutrition, bone disease, urolithiasis, and kidney failure were recognized.34Baddeley R.M. An epilogue to jejunoileal bypass.World J Surg. 1985; 9: 842-849Crossref PubMed Scopus (20) Google Scholar In this article, discussion will be limited to the renal complications of bariatric surgery. JIB was first described in the literature by Payne et al35Payne J.H. Dewind L.T. Commons R.R. Metabolic observations in patients with jejunocolic shunts.Am J Surg. 1963; 106: 273-289Abstract Full Text PDF PubMed Scopus (208) Google Scholar in 1963, but the first reports of kidney stones ascribed to the procedure did not appear until 1973.36Dickstein S.S. Frame B. Urinary tract calculi after intestinal shunt operations for the treatment of obesity.Surg Gynecol Obstet. 1973; 136: 257-260PubMed Google Scholar The delay was likely caused by the relative frequency of stone disease because stone passage engenders little suspicion of a new, more serious syndrome. Urolithiasis in patients with chronic diarrheal syndromes is well known and attributed to the following risk factors: low urine volume, low urine citrate, and low urine pH from the metabolic acidosis induced by intestinal alkali loss. Patients are predisposed to both uric acid and calcium oxalate stones.37Worcester E.M. Stones from bowel disease.Endocrinol Metab Clin North Am. 2002; 31: 979-999Abstract Full Text Full Text PDF PubMed Scopus (115) Google Scholar However, the description of enteric hyperoxaluria in patients with severe bowel disease and/or intestinal resection suggested that another mechanism might be pathogenic in JIB.38Smith L.H. Fromm H. Hofmann A.F. Acquired hyperoxaluria, nephrolithiasis, and intestinal disease. Description of a syndrome.N Engl J Med. 1972; 286: 1371-1375Crossref PubMed Scopus (211) Google Scholar Multiple reports implicated hyperoxaluria as the major lithogenic risk factor in JIB.36Dickstein S.S. Frame B. Urinary tract calculi after intestinal shunt operations for the treatment of obesity.Surg Gynecol Obstet. 1973; 136: 257-260PubMed Google Scholar, 39Requarth J.A. Burchard K.W. Colacchio T.A. et al.Long-term morbidity following jejunoileal bypass. The continuing potential need for surgical reversal.Arch Surg. 1995; 130: 318-325Crossref PubMed Scopus (128) Google Scholar, 40Nordenvall B. Backman L. Larsson L. et al.Urine composition following jejunoileal bypass.Eur Urol. 1983; 9: 35-39PubMed Google Scholar The hyperoxaluria was often severe and reached levels associated with primary hyperoxaluria, with urinary oxalate excretion rates in the range of 100 to 300 mg/d. Paradoxically, the overabsorption of dietary oxalate was the result of malabsorption of other dietary nutrients. Marked reductions of urine oxalate occurred after patients were placed on low oxalate diets and confirmed that intestinal oxalate overabsorption was the mediator of hyperoxaluria.41Stauffer J.Q. Humphreys M.H. Weir G.J. Acquired hyperoxaluria with regional enteritis after ileal resection. Role of dietary oxalate.Ann Intern Med. 1973; 79: 383-391Crossref PubMed Scopus (60) Google Scholar, 42Earnest D.L. Johnson G. Williams H.E. et al.Hyperoxaluria in patients with ileal resection: An abnormality in dietary oxalate absorption.Gastroenterology. 1974; 66: 1114-1122Abstract Full Text PDF PubMed Scopus (166) Google Scholar Oxalate overabsorption also resulted from fat malabsorption, which led to increased free fatty acid concentrations with luminal calcium complexation, thereby enhancing the bioavailabilty of oxalate for gut absorption.37Worcester E.M. 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Effects of ricinoleate and bile salts on oxalic acid and neutral sugar transport.J Clin Invest. 1984; 74: 805-811Crossref PubMed Scopus (29) Google Scholar The chronic hyperoxaluria of many JIB patients led to recurrent calcium oxalate stone formation and chronic kidney disease, with some patients progressing to end-stage renal disease. Requarth et al39Requarth J.A. Burchard K.W. Colacchio T.A. et al.Long-term morbidity following jejunoileal bypass. The continuing potential need for surgical reversal.Arch Surg. 1995; 130: 318-325Crossref PubMed Scopus (128) Google Scholar followed 453 patients for a mean follow-up of 15 years after; 29% developed kidney stones, 8% had significant loss of kidney function, and 7 patients developed end-stage renal disease.39Requarth J.A. Burchard K.W. Colacchio T.A. et al.Long-term morbidity following jejunoileal bypass. The continuing potential need for surgical reversal.Arch Surg. 1995; 130: 318-325Crossref PubMed Scopus (128) Google Scholar In that cohort, 31% required surgical revision of the JIB, not all for kidney-related problems though. In 1979, the US Food and Drug Administration banned JIB because of its many complications. However, this did not end bariatric surgery and the Roux-en-Y gastric bypass (RYGB) quickly became the procedure of choice for weight loss. Over the last 10 years, bariatric surgery has become increasingly common. The National Institutes of Health has recommended that a BMI >40 kg/m2 as 1 criterion for bariatric surgery. As can be seen in Figure 1, the prevalence of severe obesity almost doubled between 1994 and 2000. Now, nearly 5% of the adult population may be considered surgical candidates. Modern bariatric surgery consists of purely restrictive procedures and mixed restrictive and malabsorptive procedures. In restrictive procedures, such as laparoscopic stomach banding, food capacity is reduced, but there is no disruption of intestinal flow. RYGB and biliopancreatic diversion (BPD) are mixed restrictive and malabsorptive procedures.45Puzziferri N. Blankenship J. Wolfe B.M. Surgical treatment of obesity.Endocrine. 2006; 29: 11-19Crossref PubMed Scopus (21) Google Scholar Of bariatric surgeries currently practiced, RYGB accounts for approximately 70% to 80% of bariatric surgeries in the United States.46Santry H.P. Gillen D.L. Lauderdale D.S. Trends in bariatric surgical procedures.JAMA. 2005; 294: 1909-1917Crossref PubMed Scopus (774) Google Scholar In RYGB, a small stomach pouch is created to limit food intake