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PubMed2006

Disruption of clc-5 leads to a redistribution of annexin A2 and promotes calcium crystal agglomeration in collecting duct epithelial cells.

Mutations in CLCN5, which encodes the voltage-dependent Cl(-)/H(+)antiporter, CLC-5, cause Dent's disease. This disorder is characterized by low molecular-weight proteinuria, hypercalciuria, nephrocalcinosis and nephrolithiasis. Using a collecting duct cell model (mIMCD-3) in which endogenous clc-5 is disrupted by antisense clc-5 or overexpression of truncated clc-5, we demonstrate altered expression of the crystal adhesion molecule, annexin A2. Endogenously expressed annexin A2 is intracellular with limited plasma membrane localization. Following clc-5 disruption, there is both a marked increase in plasma membrane annexin A2 and an increase in cell surface crystal retention and agglomeration, which may be attenuated using pretreatment with anti-annexin A2 antibodies or wheat germ agglutinin lectin but not by concanavalin A. We hypothesize that in Dent's disease, endocytic failure leads to an accumulation at the plasma membrane of crystal-binding molecules that include annexin A2 leading to retention of calcium crystals and ultimately nephrocalcinosis and nephrolithiasis.

Animals↗

PubMed2004

Association of vitamin D receptor genotypes with calcium excretion in nephrolithiatic subjects in northern India.

Our objective was to investigate the association between the vitamin D receptor (VDR) allelic variants (Bsm I and Fok I) and nephrolithiasis in northern India. A total of 150 nephrolithiatic patients and 100 age and sex matched controls were enrolled for study. A 10 ml blood sample was obtained for biochemical analysis and DNA isolation. In addition, 24 h urine samples were obtained from each patient for the estimation of calcium and creatinine. PCR was performed for the Bsm I and Fok I VDR variants. The association between Bsm I and Fok I VDR polymorphism and nephrolithiasis was investigated after digestion with restriction enzymes (3 U). The product was analysed on 3% agarose gel for Bsm I and 15% polyacrylamide gel for Fok I allelic variants. We did not observe any significant differences in the prevalence of either the Bsm I or Fok I VDR genotypes between stone formers and controls. The B allele was found to be more prevalent in hypercalciuric patients compared to controls and nephrolithiatic subjects. The subjects with the bb genotype exhibited a higher calcium excretion than the BB genotype. Patients with the F allele were also found to excrete higher urinary calcium. VDR genotypes may be associated with increased calcium excretion in hypercalciuric nephrolithiatic subjects.

Adolescent↗

PubMed2006

Artificial neural networks for assessing the risk of urinary calcium stone among men.

The pathophysiology of idiopathic calcium oxalate nephrolithiasis involves metabolic abnormalities. Previous studies gave conflicting results about the metabolic factors in stone formers. Artificial neural networks (ANN) are new methods based on computer programming that have outperformed conventional methods in prediction of outcomes in different medical applications. The aim of our study was to compare with ANN the clinical and biochemical parameters implicated in urinary calcium stone between stone formers (SF) and controls (C). We compared 11 clinical and biochemical variables among 119 male idiopathic calcium oxalate SF and 96 C by univariate and multivariate statistical analyses. Univariate analyses included discriminant analysis, logistic regression analysis, and ANN. For multivariate analyses, stepwise discriminant analysis and ANN were performed. Variables included age, body mass index (BMI), family history of nephrolithiasis, supersaturation with respect to calcium oxalate, calcemia, and 24-h urinary calcium, oxalate, uric acid, urea, sodium, and citrate. With univariate and multivariate analyses, ANN were as efficient as classical statistical analyses in discriminating the different parameters. The sensitivity, the specificity, and the percentage of correctly classified patients were similar in all analyses. With ANN, supersaturation (receiver operating characteristic, ROC curves index 0.73) and urea (ROC 0.72) were the most discriminant followed by family history and urinary calcium (ROC 0.67). ROC index was 0.63 for citrate, 0.61 for oxalate and urate, 0.60 for sodium and calcemia, 0.58 for age, and 0.56 for BMI, but these parameters were not statistically different between SF and C. ANN gave additional information since they made it possible to determine the cut-off values of the parameters and their predictive power. Cut-off values for being a stone former were 8.9 for supersaturation and 363 mmol/day for urinary urea with a predictive power of 0.69 and 0.70, respectively. Univariate and multivariate analysis evidenced supersaturation and 24-h urinary urea excretion as the most discriminant parameters between the two populations. In addition to high supersaturation, the negative impact of protein intake was confirmed.

Adolescent↗

PubMed2006

Continuous infusion of oxalate by minipumps induces calcium oxalate nephrocalcinosis.

It is hypothesized that oxalate plays an active role in calcium oxalate (CaOx) nephrocalcinosis and oxalate driven nephrolithiasis by interacting with the kidney. We developed an adjustable, nonprecursor, continuous infusion model of hyperoxaluria and CaOx nephrocalcinosis to investigate this hypothesis. Minipumps containing PBS or KOx (60-360 micromol/day; n = 5-7/dose) were implanted subcutaneously in male Sprague-Dawley rats on D0 and D6. Rats were killed on D13. Oxalate excretion and CaOx crystalluria were monitored by 20+4 h urine collections. Localization and content of intrarenal crystals were determined on frozen sections using polarization and microFTIR. Oxalate excretion was significantly elevated in all KOx rats (P < or = 0.005). CaOx crystalluria was most persistent in the 240-360 micromol/day KOx rats, but even 60 micromol/day KOx rats showed sporadic crystalluria. One hundred percent of KOx rats had CaOx nephrocalcinosis as confirmed by microFTIR. Most crystals were localized to the lumens of the corticomedullary collecting ducts. A few crystals are localized just under the papillar urothelium. The minipump model is the first model of hyperoxaluria to provide continuous infusion of oxalate. It permits control of the levels of hyperoxaluria, crystalluria and CaOx nephrocalcinosis. The level of sustained hyperoxaluria and CaOx nephrocalcinosis induced by treatment with 360 micromol/day KOx for 13D models the conditions frequently observed in jejunoileal bypass patients. Adjustments in the length of treatment and level of hyperoxaluria may allow this model to also be used to study the oxalate driven CaOx-nephrolithiasis common in patients with hyperoxaluria due to other causes.

Animals↗

PubMed1997

A second family with XLRH displays the mutation S244L in the CLCN5 gene.

Mutations in the CLCN5 gene, mapped in Xp11.22, have been recently reported to be associated with X-linked nephrolithiasis, X-linked recessive hypophosphataemic rickets and Dent's disease. We report a missense mutation in exon 6 of the CLCN5 gene. The mutation in this pedigree is S244L, the same mutation as has previously been described in an Italian family showing a similar pathology. However, in the family reported here, affected males have developed neither nephrolithiasis nor nephrocalcinosis. The question arises whether we are dealing with a milder phenotype or whether a more severe pathology will develop with ageing.

Adolescent↗

PubMed2002

Primary hyperoxaluria type 2 in children.

The primary hyperoxalurias (PH1 and PH2) are rare defects of oxalate overproduction. There are only 24 reported cases of PH2, which is characterized by raised urine oxalate and L-glycerate. We describe 13 previously unreported children with PH2, representing the largest single-centre cohort in the world. DNA samples were tested for a common mutation and four other documented mutations in the gene encoding the enzyme glyoxylate reductase/hydroxypyruvate reductase (GRHPR). Two of the five kindred showed homozygosity for two different mutations in the GRHPR gene. The genetic defect was not identified in the other three families. The median age at diagnosis of PH2 was 1.7 years. Five children presented with nephrolithiasis between 0.8 and 9 years. Haematuria was common, but urinary tract infection and nephrocalcinosis were not. All had normal renal function at diagnosis, and only 1 patient had a significant decline in glomerular filtration rate. We conclude that all children with nephrolithiasis secondary to hyperoxaluria should have urinary glycerate measured, as PH2 may be more prevalent than currently estimated. DNA mutational analysis may be useful in supporting the diagnosis.

Adolescent↗

PubMed2005

Eighteen-year follow-up of a patient with partial hypoxanthine phosphoribosyltransferase deficiency and a new mutation.

Hypoxanthine phosphoribosyltransferase (HPRT) deficiency is an inherited disorder. Complete deficiency of HPRT activity is phenotypically expressed as the devastating Lesch-Nyhan syndrome. Partial HPRT deficiency usually causes hyperuricemia, precocious gout, and uric acid nephrolithiasis. We describe an 18-year follow-up of a 5-year old boy with partial HPRT deficiency and report a novel mutation in his HPRT gene. He presented with overproduction of uric acid and passage of uric acid renal stones, and without gout or neurological and behavioral abnormalities. Treatment with allopurinol, adequate hydration, urinary alkalization, and a low-purine diet was started. No subsequent nephrolithiasis has occurred. After 18-year of this therapy his physical and neuropsychological status were normal, merely his glomerular filtration rate (GFR, normal 97-137 mL min(-1)/1.73 m(2)) fell from normal to 65.1 mL min(-1). The most likely cause of initial renal impairment in our patient is uric and/or xanthine crystalluria. A missense and transition mutation 169A>G (57ATG>GTG, 57met>val) in exon 3 of the patient's HPRT gene was identified and the mother was the carrier of the mutation. As far as we are aware, the identified mutation has not previously been reported. We named the mutant HPRT Maribor.

Allopurinol↗

PubMed2000

Clinical presentation and natural course of idiopathic hypercalciuria in children.

Idiopathic hypercalciuria (IHC) has been reported mainly in children with hematuria in the 1980s and early 1990s, when renal sonography was just becoming routine. The presence of microcalculi, i.e., of hyperechogenic spots < 3 mm in diameter in renal calyces, was not taken into account in those studies. We attempted to outline clinical presentation and natural course of IHC not only in children with hematuria, but also in those with dysuria and/or recurrent abdominal/flank pain and a family history of nephrolithiasis, taking into account the finding of microcalculi. We analyzed retrospectively the data at diagnosis from 74 consecutive children aged 2.4-18 years (mean 8.6) with IHC (calciuria 4.1-15.1 mg kg-1 24 h-1, mean 6.1) and the outcome of 30 of them who were followed > or = 1 years (mean 3.2) with no specific therapy. At diagnosis, 38 patients (51%) had no hematuria, 42 (57%) had microcalculi and four (5%) had calculi. Of the patients with normal urinalysis, 71% had microcalculi or stones. The subjects with microcalculi and those with stones were significantly older than those without microcalculi and stones (P = 0.004 and 0.007). A normal urinalysis at our evaluation and a history of abdominal/flank pain were significantly more frequent in patients with microcalculi than in those without (P = 0.02 and 0.0001, respectively). During the follow-up, four of 30 patients formed stones 1-3 years after first diagnosis of IHC. More than half of children with IHC have microcalculi. The risk of formation of microcalculi or stones increases with age. The lack of hematuria does not exclude the presence of microcalculi or calculi. Hypercalciuria has to be suspected in children with dysuria and/or recurrent abdominal flank pain and a family history of nephrolithiasis, even when they have no hematuria.

Abdominal Pain↗

PubMed2000

Atypical distal renal tubular acidosis confirmed by mutation analysis.

In autosomal dominant distal renal tubular acidosis type I (dRTA) impaired hydrogen ion secretion is associated with metabolic acidosis, hyperchloremic hypokalemia, hypercalciuria, nephrocalcinosis, and/or nephrolithiasis. A retardation of growth is commonly observed. In this report we present a family with autosomal dominant dRTA with an atypical and discordant clinical picture. The father presented with severe nephrocalcinosis, nephrolithiasis, and isosthenuria but metabolic acidosis was absent. His 6-year-old daughter, however, suffered from metabolic acidosis, hypokalemia, and hypercalciuria. In addition, sonography revealed multiple bilateral renal cysts but no nephrocalcinosis. Mutation analysis of the AE1 gene coding for the renal Cl-/HCO3(-)-exchanger AE1 displayed a heterozygous Arg589Cys exchange in both patients but not in the healthy family members. This point mutation is frequently associated with autosomal dominant dRTA. Diagnosis of autosomal dominant dRTA is supported in this family by results of AE1 mutation analysis.

Acidosis, Renal Tubular↗

PubMed2002

Renal Dysfunction in HIV-1-infected Patients.

Improved therapy directed against opportunistic infection and HIV-1 itself has resulted in greatly enhanced patient survival in the past decade among patients infected with HIV-1. Since patients are living longer, HIV-1 infection is associated with a rising burden of kidney disease. Approximately 14% of black patients and 6% of white patients dying with HIV-1 infection in 1999 in the United States had renal disease. Overall, 10% of patients dying with HIV-1 infection had renal failure. The most common glomerular diseases are focal segmental glomerulosclerosis and immune complex glomerulonephritis. Appropriate therapy for focal segmental glomerulosclerosis includes effective antiretroviral therapy and angiotensin antagonist medication. Drug toxicity is also common, often manifesting as electrolyte abnormalities, acute renal failure, interstitial nephritis, or nephrolithiasis. In particular, indinavir is associated with crystalluria, nephrolithiasis, interstitial nephritis, and lower urinary tract inflammation. Appropriate screening for renal disease and appropriate intervention will likely reduce the morbidity and mortality associated with progressive renal disease.

Journal Article↗

PubMed1975

Calculi complicating a renal transplant.

Four months after a cadaver kidney transplant, kidney stones were found in the renal allograft. Three major predisposing causes of nephrolithiasis were found in the patient, including hyperparathyroidism, renal tubular acidosis, and urinary tract infection. Hypercalcemia was corrected by parathyroidectomy. During the subsequent three years there was no enlargement of the renal stones and adequate kidney function was maintained. Renal tubular acidosis was not severe and seemed to be related to chronic rejection. Urinary tract infection was readily corrected with antibiotics and did not recur after the immediate post-transplant period. Surgical therapy for nephrolithiasis involving a kidney allograft was defferred since urinary flow was not obstructed. This course of management is recommended for use in patients with calculi complicating renal transplantation.

Acidosis, Renal Tubular↗

PubMed1981

Increased urine angiotensin I converting enzyme activity in patients with upper urinary tract infection.

Angiotensin converting enzyme (ACE) is present within the brush border of the tubular cell of the kidney. Since it has a high molecular mass, ACE activity of urine most probably derives only from tubular cells, thus suggesting the potential usefulness of ACE determination as an index of tubular damage. When assayed with the method described, ACE is optimally active at pH 8 with a calcium concentration exceeding 0.75 mmol/l urine, and is chloride independent. Urine dialysis has no effect on ACE activity. ACE is stable at 4 degrees C for 10 days, but it is inactivated by repeated thawing and freezing. The presence of leucocytes and bacteria does not interfere with the assay. Urine ACE activity was evaluated in patients with upper and lower urinary tract infection, nephrolithiasis, chronic glomerulonephritis and essential hypertension and was found to be significantly increased only in patients affected by upper urinary tract infection and nephrolithiasis.

Calcium↗

PubMed1987

Urinary excretion of glycosaminoglycans in urological disease.

Altered urinary excretion of glycosaminoglycans (GAG) has been reported in patients with nephrolithiasis, with chronic glomerulonephritis, and incipient diabetic nephropathy, but evaluation of urinary GAG has not been reported in infections and proliferating diseases of the urinary tract. Urinary excretion of GAG was measured in 50 patients with idiopathic calcium nephrolithiasis (ICN) of whom 20 had associated urinary tract infection, in 20 subjects with recurrent infection of the urinary tract (UTI), and in 18 patients with bladder papillomatosis. Mean values were significantly lower in ICN, increased in papillomatosis, and in the normal range in UTI.

Diabetic Nephropathies↗

PubMed1977

Effect of hydrochlorothiazide therapy on the crystallization of calcium oxalate in urine.

The effect of hydrochlorothiazide on the formation of renal stones was evaluated by quantitative assessment of the propensity of urine to undergo crystallization of calcium oxalate. In seven patients with calcium urolithiasis (three with absorptive hypercalciuria, one with renal hypercalciuria, and three with normocalciuric nephrolithiasis), the urinary activity product ratio and formation product ratio of calcium oxalate were measured both on and off therapy with hydrochlorothiazide (50 mg orally twice a day). The activity product ratio (state of saturation with respect to calcium oxalate) decreased in the majority of cases, primarily as a result of the fall in urinary calcium. The formation product ratio (limit of metastability) increased in all cases; the cause of the increase was not readily apparent. Both changes reduced the propensity of urine to undergo crystallization of calcium oxalate, and therefore may account for the clinical improvement reported during thiazide therapy in nephrolithiasis.

Adult↗

PubMed2004

Effects of escin on indinavir crystallization time in the urine of patients with HIV-I infection: a multicenter, randomized, open-label, controlled, four-period crossover trial.

BACKGROUND: The combination of indinavir, a protease inhibitor, and reverse-transcriptase inhibitors is widely used in the treatment of HIV-1 infection. However, precipitation of indinavir crystals in the renal tubular lumen due to the drug's aqueous insolubility may result in characteristic symptoms of flank pain or classic renal colic. An in vitro study has shown that addition of escin to synthetic urine containing indinavir delayed the crystallization time of indinavir. OBJECTIVE: This study examined the efficacy and tolerability of the addition of escin to highly active antiretroviral therapy containing indinavir to delay the crystallization time of indinavir in urine. METHODS: This was a multicenter, randomized, open-label, controlled, 4-period crossover trial in which each period lasted 4 weeks. HIV-1-infected adults receiving treatment with indinavir plus 2 nucleoside analogue reverse-transcriptase inhibitors in whom plasma viral loads had been undetectable (HIV-1 RNA <200 copies/mL) for at least 6 months were randomly assigned to 1 of 2 groups based on the timing of the initiation of escin. Group I received escin during the second and third treatment periods, and group II received escin during the first and fourth treatment periods. The primary end point was the in vitro crystallization time of indinavir in 24-hour urine specimens, determined at the end of each 4-week period. Tolerability was assessed based on the number of patients with a rebound in plasma viral load and on the numbers of clinically and biologically relevant adverse events (including those requiring discontinuation of treatment). Clinical and laboratory evaluations were performed throughout each 4-week period. RESULTS: Fifty HIV-1-infected patients were enrolled, 47 were randomized to treatment (40 [85.1%] men, 7 [14.9%] women; median [interquartile range] age, 36 [34-45] years), and 30 completed the study. Urine pH and plasma and urine indinavir concentrations were unaffected by the addition of escin to antiretroviral treatment. The mean time to the onset of crystallization was 14.7 minutes with escin (95% Cl, 11.8-17.5) and 9.9 minutes without it (95% Cl, 6.7-13.1). Therefore, the addition of escin increased the mean crystallization time by 5.5 minutes (95% Cl, 1.5-9.5; P = 0.008), representing the overall capacity of study treatment to inhibit indinavir crystallization in the urine. Three of 47 patients had mild gastrointestinal symptoms associated with escin treatment. No episodes of nephrolithiasis were recorded during the study or after the completion of study treatment. CONCLUSION: The results of this prospective clinical trial of the effect of escin on indinavir crystallization time support the possibility that indinavir-associated nephrolithiasis may be prevented by means other than overhydration. Further research is needed in greater numbers of patients over longer follow-up times.

Adult↗

PubMed2005

Credentials of Spirulina diet on stability and flux related properties on the biomineralization process during oxalate mediated renal calcification in rats.

BACKGROUND: High Spirulina diet is a potential risk factor for nephrolithiasis since it has the capacity to increase urinary oxalate and uric acid level, facilitating lithogenesis. Our aim was to identify the effect of Spirulina diet during hyperoxaluric condition in Wistar albino rats. METHODS: The animals were divided into four groups: control (Gl, n=6); ethylene glycol (EG) induced (G2, n=6); EG+Spirulina (G3, n=6); Spirulina alone (G4, n=6). EG at 0.75% was administered to G2 and G3 through drinking water for 4 weeks and Spirulina 1500 mg/kg feed was administered to G3 and G4. RESULTS: Urinary parameters like oxalate, uric acid, calcium, urea, and creatinine (P<0.001) were found increased after Spirulina diet under hyperoxaluric conditions compared to the same without Spirulina diet. Similarly the BUN, plasma contents of uric acid, urea, creatinine (P<0.001) were found to be raised in G3. The renal and RBC GSH levels, as estimated by HPLC, seemed decreased when compared to G2. CONCLUSIONS: The present study shows that free radicals aid in the progression of nephrolithiasis. The crystal deposition was found to be high in the renal cells of G3 than G2 and TEM revealed damage in renal cell of G3 implying that the disease deteriorates by free radical injury. In contrast the Spirulina diet alone (G4) did not induce any features relating to stone forming condition suggesting that free radical release might have been suppressed due to enrichment of dietary antioxidants and vitamins. Thus the present investigation demonstrates that during hyperoxaluric conditions the Spirulina diet must possibly be avoided and can be considered in normal subjects checked for family history of renal stone deposition.

Animals↗

PubMed2025

Outcome of conservative management of small renal stones in prepubertal children.

INTRODUCTION: Renal stones are relatively uncommon in the pediatric population. This study aimed to evaluate the utility of conservative management of small renal stones in prepubertal children. PATIENTS AND METHODS: A retrospective chart review was conducted for children (≤12 years old) with small renal stones (3-10 mm) from 2016 to 2023 who underwent conservative management. Management included periodic renal ultrasonography, every 6 months, in addition to good hydration. Stones were confirmed by two consecutive ultrasounds. We recorded the patient's demographics and ultrasound findings (stone side, size, laterality, location, number, and associated hydronephrosis). Surgical intervention was indicated if recurrent loin pain, recurrent UTI, or worsening hydronephrosis (obstructing stone). Nephrolithiasis was considered resolved if stones were not visualized on 2 consecutive ultrasounds. Moreover, we evaluated conservative management outcomes for those presented during infancy (<12 months) versus later. RESULTS: We included 52 patients (65renal units) who presented at a median age of 46.1months (5.3-155.1). Seventy-five percent of patients had incidental renal stones. The median stone size was 4 mm (3-10). Forty-six percent of stones were in the lower calyx. The majority (70.8 %) had no hydronephrosis at presentation. During a median follow-up of 39months, 15patients with 17units (26.2 %) were documented stone-free. Ten patients (19.2 %) had symptomatic stone events, all measured ≥4 mm. Of them, 6 patients (6 units) underwent surgical interventions, and 4 patients (4 units) experienced complications. A ROC curve analysis identified a stone size cutoff of 4 mm (sensitivity 100 % and 29 % specificity) that could be associated with symptomatic stone events. Using a multivariate Cox regression model, stone size was the only significantly associated factor with subsequent surgical intervention (p = 0.007). 19 % (10patients,12units) presented during infancy. Notably, the incidence of stone-free rate was significantly higher during infancy compared to older children (58.3 % vs 18.9 %,respectively). DISCUSSION: During a 39-month follow-up, 4 patients developed complications (2recurrent pain and 2 experienced UTI), supporting the safety of conservative management of small renal stones. This study is limited due to its retrospective design and the reliance on ultrasound as the main imaging method. To minimize that, all ultrasound images were carefully reviewed by two pediatric urologists. Moreover, renal stones were confirmed using strict criteria, which required detection in two consecutive ultrasounds. CONCLUSION: Although 26.2 % of units had spontaneously resolved nephrolithiasis, surgical intervention was only required in 11.5%of patients, all of whom had renal stones≥4 mm. Infants had higher spontaneous resolutions without complications, suggesting that conservative management may be especially effective in this subgroup.

Humans↗

PubMed2007

Hyperoxaluria in kidney stone formers treated with modern bariatric surgery.

PURPOSE: Nephrolithiasis and renal failure secondary to severe hyperoxaluria were complications of jejunoileal bypass for obesity, leading to the discontinuation of this procedure in the United States in 1980. Bariatric procedures currently in use have not been adequately evaluated for this complication. MATERIALS AND METHODS: We compared 24-hour urine chemistry studies of 132 patients with nephrolithiasis who had undergone bariatric surgery with the urine chemistry studies of patients who had undergone jejunoileal bypass, those with routine kidney stones and normal subjects. The primary aim was to determine if hyperoxaluria developed in patients who underwent bariatric surgery and had kidney stones as had been seen with jejunoileal bypass. RESULTS: Patients who have undergone modern bariatric surgery had an adjusted mean urine oxalate excretion of 83 mg per day compared to 39 mg per day for routine kidney stone formers and 34 mg per day for normal subjects (p <0.001 for both comparisons), but not quite as high as that found in patients treated with jejunoileal bypass (102 mg per day, p <0.001). Urine supersaturation of calcium oxalate, the main driving force for calcium oxalate stone formation, was higher in patients treated with bariatric surgery compared to routine kidney stone formers and normal subjects (p <0.001 for both comparisons). CONCLUSIONS: Hyperoxaluria is the most significant abnormality of urine chemistry studies in patients with kidney stones who have undergone bariatric surgery. Many of these patients have a degree of hyperoxaluria that could lead to kidney failure. Further studies are required to determine the prevalence of this problem in patients who have undergone bariatric surgery.

Bariatric Surgery↗