Dietary Recommendations for Bariatric Patients to Prevent Kidney Stone Formation
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nutrients Review Dietary Recommendations for Bariatric Patients to Prevent Kidney Stone Formation 1, 1,2, 1,2, Milene S. Ormanji y , Fernanda G. Rodrigues y and Ita P. Heilberg * 1 Nephrology Division, Universidade Federal de São Paulo, São Paulo 04023-062, Brazil; [email protected] (M.S.O.); [email protected] (F.G.R.) 2 Department of Nutrition, Universidade Federal de São Paulo, São Paulo 04023-062, Brazil * Correspondence: [email protected]; Tel.: +55-(11)-5576-4848 (ext. 2465) Contributed equally. y Received: 27 April 2020; Accepted: 13 May 2020; Published: 16 May 2020 Abstract: Bariatric surgery (BS) is one of the most common and efficient surgical procedures for sustained weight loss but is associated with long-term complications such as nutritional deficiencies, biliary lithiasis, disturbances in bone and mineral metabolism and an increased risk of nephrolithiasis, attributed to urinary metabolic changes resultant from low urinary volume, hypocitraturia and hyperoxaluria. The underlying mechanisms responsible for hyperoxaluria, the most common among all metabolic disturbances, may comprise increased intestinal oxalate absorption consequent to decreased calcium intake or increased dietary oxalate, changes in the gut microbiota, fat malabsorption and altered intestinal oxalate transport. In the current review, the authors present a mechanistic overview of changes found after BS and propose dietary recommendations to prevent the risk of urinary stone formation, focusing on the role of dietary oxalate, calcium, citrate, potassium, protein, fat, sodium, probiotics, vitamins D, C, B6 and the consumption of fluids. Keywords: nephrolithiasis; bariatric surgery; hyperoxaluria; kidney stones; diet 1. Introduction Obesity is one of the most important worldwide public health challenges predisposing to severe comorbidities such as diabetes mellitus, cardiovascular disease, cancer, sleep apnea and hypertension [1]. Considering the difficulties regarding diet therapy as a long-term control of morbid obesity, bariatric surgery (BS) translated into an efficient method for sustained weight loss [2]. BS procedures comprise restrictive techniques like gastric banding and sleeve gastrectomy, malabsorptive techniques such as biliopancreatic diversion and duodenal switch, or a combination of both as in a Roux-en-Y gastric bypass (RYGB), one of the most common surgical procedures performed over the last years. Although BS is considered an efficacious technique with benefits concerning the treatment of comorbidities of the morbidly obese patients, it may bring long-term complications such as nutritional deficiencies, biliary lithiasis, disturbances in bone and mineral metabolism and an increased risk of nephrolithiasis [3,4]. Such a risk is estimated to be around 7.6% in bariatric patients until 5 years after surgery, which represents almost a two-fold increase in risk if compared with morbidly obese patients [5,6], showing the greatest risk in malabsorptive procedures, intermediate risk in standard RYGB, and the least risk in restrictive techniques [7]. Nephrolithiasis arises from urinary metabolic changes in these patients, such as low urinary volume, hypocitraturia and hyperoxaluria. As a rule, hyperoxaluria may be due to the rare monogenic disorders of primary hyperoxaluria, characterized by increased production of endogenous oxalate within the liver consequent to the various mutations as opposed to secondary hyperoxaluria, ascribed to excessive oxalate intake or increased intestinal absorption (enteric). Secondary hyperoxaluria is Nutrients 2020, 12, 1442; doi:10.3390/nu12051442 www.mdpi.com/journal/nutrients Nutrients 2020, 12, 1442 2 of 15 Nutrients 2020, 12, x FOR PEER REVIEW 2 of 16 certainly the case in patients that have undergone BS and represents the most frequent metabolic disturbanceSecondary hyperoxaluria detected among is them,certainly with the prevalence case in patients rates ranging that have from undergone 29% to around BS and 67% represents at 3 months the andmost 2 frequent years after metabolic BS [8–11 disturbance]. A recent detected meta-analysis among hasthem, demonstrated with prevalence a 36.4% rates increase ranging infrom urinary 29% oxalateto around levels 67% after at 3 BS months considering and 2 theyears 24-h after urine BS profile [8–11] from. A recent 277 patients meta-analysis belonging has to demonstrated six prospective a studies36.4% increase after almost in urinary 1 year ofoxalate RYGB levels [12]. after BS considering the 24-hour urine profile from 277 patientsThe belonging underlying to mechanismssix prospective for studies an increasing after almost urinary 1 year oxalate of RYGB in post-BS[12]. patients have not been completely elucidated but may be accounted for dietary factors, intestinal fat malabsorption, alterations in gut microbiota, and/or changes in the intestinal oxalate transport [13], as hypothesized in Figure1 below: FigureFigure 1.1. HypotheticalHypothetical underlying mechanisms for hyperoxaluria after bariatric surge surgeryry (BS) (BS).. A diet richrich inin oxalateoxalate oror poorpoor inin calciumcalcium contentcontent decreasesdecreases thethe amountamount of poorly soluble, nonabsorbable calciumcalcium oxalateoxalate (CaOx)(CaOx) complexescomplexes inin thethe intestinal lumen leading to a higher amount of free free oxalate forfor absorption.absorption. Vitamin Vitamin C (ascorbic acid) s supplementsupplements are metabolized to oxalate contributing to hyperoxaluria.hyperoxaluria. BS predisposes to the development of fat malabsorption, which which in in the presence of of a a highhigh dietarydietary fatfat intake intake further further enhances enhances free free oxalate oxalate absorption absorption due due to to the the sequestration sequestration of of calcium calcium by fat.by fat. The The increased increased intestinal intestinal exposure exposure to to complexes complexes of of unconjugated unconjugated bile bile salts salts andand fattyfatty acids could could aaffectffect microbiotamicrobiota compositioncomposition andand alsoalso decreasedecrease thethe colonization by Oxalobacter formigenes and other oxalate-degradingoxalate-degrading bacteria.bacteria. Increased gut permeability induced by excessive unconjugated bile salts andand otherother factorsfactors may occur. Finally, changes in intestinal oxalate transporters could lead to to increased increased netnet intestinalintestinal oxalateoxalate absorption.absorption. AA dietdiet richrich inin oxalateoxalate andand/or/or poorpoor inin calciumcalcium decreases the generation of unabsorbable calcium oxalateoxalate (CaOx)(CaOx) complexes complexes ultimately ultimately leading leading to ato higher a higher amount amount of free of oxalatefree oxalate in the in intestinal the intestinal lumen. Inlumen. a previous In a previous study conducted study conducted by our group by our [14 group], an exaggerated [14], an exaggerated oxaluric responseoxaluric wasresponse observed was followingobserved anfollowing oral oxalate an oral load oxalate in 61 post-BS load in patients 61 post (58-BS RYGBpatients and (58 3 biliopancreatic RYGB and 3 biliopancreatic diversion with duodenaldiversion switch)with duodenal compared switch) to morbidly compared obese to morbidly patients obese and also patients to their and own also urinary to their oxalate own urinary levels 6oxalate months levels before 6 themonths procedure, before suggestingthe procedure, an increased suggesting absorption an increased of dietary absorption oxalate of as dietary a predisposing oxalate mechanismas a predisposing for enteric mechanism hyperoxaluria. for enteric hyperoxaluria. TheThe occurrenceoccurrence ofof hyperoxaluriahyperoxaluria following BS can be also associated with increased fecal fat malabsorption,malabsorption, probablyprobably duedue toto thethe higher amount of unabsorbed bile and fatty fatty acids acids which which saponify saponify intestinalintestinal calcium,calcium, limitinglimiting thethe amountamount ofof luminalluminal free-calciumfree-calcium bindingbinding withwith oxalateoxalate [ 15[15––1818]]. AlterationsAlterations inin intestinalintestinal microbiota induced by the intestinal bypass such such as as a a reportedly reducedreduced colonizationcolonization byby OxalobacterOxalobacter formigenesformigenes,, commensalcommensal Gram-negativeGram-negative anaerobic bacteria with naturally-occurringnaturally-occurring oxalate oxalate metabolizing metabolizing properties properties [19– 21[19],– could21], could also contribute also contribute to increased to increase oxaluriad afteroxaluria BS. However,after BS. However, the effects the of effectsO. formigenes of O. formigenesintestinal intestinal colonization colonization upon urinary upon urinary oxalate oxalate remain controversialremain controversial [22] both [ in22 experimental] both in experiment and clinicalal and settings. clinical In ansettings. experimental In an experimental model of hyperoxaluric model of hyperoxaluric RYGB in rats, animals colonized with O. formigenes were able to reduce 74% of their urinary oxalate [23]. However, although a clinical study has shown that the colonization with O. Nutrients 2020, 12, 1442 3 of 15 RYGB in rats, animals colonized with O. formigenes were able to reduce 74% of their urinary oxalate [23]. However, although a clinical study has shown that the colonization with O. formigenes has been associated with a substantial reduction in the risk of recurrent stone formation among non-obese patients, urinary oxalate did not differ with