MOx Diet for Enteric Hyperoxaluria
Palo Alto (17 mi)Overseen byDavid Goldfarb, MD
Age: 18+
Sex: Any
Travel: May be covered
Time Reimbursement: Varies
Trial Phase: N/A
Recruiting
Sponsor: NYU Langone Health
No Placebo Group
Trial Summary
What is the purpose of this trial?This trial involves participants eating high oxalate foods and taking a specific substance to study how their bodies handle oxalate. It targets patients with IBD, post-RYGB patients with kidney stones, and healthy individuals. Researchers will collect various samples to understand oxalate processing.
Is the MOx Diet a promising treatment for enteric hyperoxaluria?The MOx Diet, which is a moderately high oxalate diet, is not highlighted as a promising treatment for enteric hyperoxaluria in the provided research. Instead, a low-oxalate diet is shown to be effective in reducing urinary oxalate levels, which can help prevent kidney stones. Other treatments like oral calcium supplements and vitamin B6/magnesium supplementation are also mentioned as beneficial.12567
What safety data is available for the MOx Diet treatment?The available studies do not directly address the safety of the MOx Diet specifically. However, related research on dietary interventions for hyperoxaluria, such as low-oxalate diets, indicates that these diets can effectively reduce urinary oxalate levels without significant adverse effects. The study on idiopathic hyperoxaluria treatments found no significant adverse events in any treatment groups, suggesting that dietary modifications, including those involving oxalate intake, are generally safe. Further research is needed to specifically evaluate the safety of the MOx Diet.13467
What data supports the idea that MOx Diet for Enteric Hyperoxaluria is an effective treatment?The available research shows that a low-oxalate diet can effectively reduce urinary oxalate levels, which is important for managing enteric hyperoxaluria. In one study, patients on a low-oxalate, low-fat diet saw their urinary oxalate levels decrease from 1.1 to 0.7 mmol/24 h. Another study found that a low-oxalate diet was more effective than vitamin B6 and magnesium supplements in reducing urinary oxalate levels, with a 31.1% reduction compared to 16.0% for supplements. This suggests that dietary changes can be a more effective treatment than supplements for reducing oxalate levels in patients with this condition.12678
Do I have to stop taking my current medications for the trial?The trial protocol does not specify if you need to stop taking your current medications. However, healthy controls must not be on any chronic medications.
Eligibility Criteria
Adults aged 18-80 with IBD or post-RYGB surgery, who've had a kidney stone or related event in the last three years can join. It's open to all races and genders but not for pregnant/nursing women, those with recent antibiotics use, colectomy patients, active IBD flare-ups, or significantly impaired kidney function.Inclusion Criteria
I am between 18 and 80 years old.
Exclusion Criteria
My kidney function, measured by eGFR, is below 60 ml/min/1.73 m2.
I have not been frequently taking antibiotics for perianal disease.
I have had all or part of my colon removed.
Treatment Details
The trial tests how a high oxalate diet affects individuals with Enteric Hyperoxaluria compared to healthy controls. Participants will follow specific diets and undergo stool and urine collections, blood tests, and intestinal health assessments at Weil Cornell Medicine.
2Treatment groups
Experimental Treatment
Active Control
Group I: Enteric HyperoxaluriaExperimental Treatment1 Intervention
Group II: Healthy ControlsActive Control1 Intervention
Find a clinic near you
Research locations nearbySelect from list below to view details:
NYU Langone HealthNew York, NY
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Who is running the clinical trial?
NYU Langone HealthLead Sponsor
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Collaborator
References
Low-oxalate, low-fat dietary regimen in hyperoxaluria following jejunoileal bypass. [2013]Previous studies have shown that the severity of enteric hyperoxaluria can be reduced in hospitalized patients who receive a diet low in oxalate and fat. Little is known of the value of such a diet in the patients' home conditions. Ten patients with hyperoxaluria (greater than 0.45 mmol/24 h) following jejuno-ileal bypass were therefore studied while on their ordinary diet and also on a diet with low-oxalate, low-fat content. The mean urinary excretion of oxalate decreased during the dietary treatment from 1.1 to 0.7 mmol/24 h. The diet was demanding, though not unfeasible for the patients. Careful and regular dietary information, preferably by a dietitian, is recommended in such cases.
Oral calcium supplement decreases urinary oxalate excretion in patients with enteric hyperoxaluria. [2017]We studied the effect of oral calcium supplementation in patients with enteric hyperoxaluria. Three patients with renal stone events following ileal resection were given oral calcium supplement. One of the three patients was put on a low-fat diet. The treatment reduced urinary oxalate excretion to the normal range. Subsequently, 2 patients reduced the dose of calcium supplementation at their own discretion and consequently developed renal stones again together with hyperoxaluria. Based on these observations, we believe that an adequate dose of calcium can normalize urinary oxalate excretion.
Plasma oxalate level in pediatric calcium stone formers with or without secondary hyperoxaluria. [2021]Plasma oxalate (POx) concentration is significantly elevated in primary hyperoxaluria, severe renal failure or ethylene glycol poisoning. In these conditions, the degree of hyperoxalemia correlates with the severity of systemic calcium oxalate (CaOx) deposition and should be therefore carefully monitored. Although secondary hyperoxaluria (secHyOx) is a common finding in pediatric patients with kidney stone disease, very little is known about POx in this condition. We therefore evaluated POx level in 59 children and adolescence with calcium urolithiasis (34 confirmed by CaOx stone analysis and 25 children with a strong clinical suspicion of this type of urolithiasis), with or without "mild" secHyOx. A control group consisted of 41 healthy sex- and age-matched children. We found that POx was significantly increased in children with calcium urolithiasis and secHyOx compared to healthy children (9.16 +/- 3.60 vs. 6.42 +/- 2.53 micromol/l), but that was not the case in children with calcium urolithiasis but with normal urinary oxalate excretion (7.12 +/- 3.33 micromol/l). We conclude that POx may be slightly increased in some pediatric calcium stone formers with secHyOx, probably related to intestinal oxalate hyperabsorption.
Recurrence of Hyperoxaluria and Kidney Disease after Combined Intestine-Kidney Transplantation for Enteric Hyperoxaluria. [2018]Enteric hyperoxaluria (EH) occurs with a rate of 5-24% in patients with inflammatory bowel disease, ileal resection and modern bariatric surgery. The excessive absorption of calcium oxalate causes chronic kidney disease (CKD) in patients with EH. In the literature, a single experience was reported in combined intestine-kidney transplantation (CIKTx) in patients with CKD due to EH.
[The Hyperoxalurias]. [2017]Oxalate (Ox) is an end-product of metabolism, important for poor solubility of its calcium salt in biological fluids. Ox can therefore be found in about 70% of urinary calculi. Hyperoxaluria (HOx) defined as Ox exceeding 0.5 mmol)/day, may cause nephrolithiasis/nephrocalcinosis and may be classified as dietary (DH), enteric (EH) or primary (PH). Fractional intestinal absorption of Ox is less than 10%, but increases to over 20% at calcium intakes below 200 mg/day. DH is often related to low-calcium diets. EH is caused by non-absorbed fatty acids which bind to calcium and lower its concentration in the intestinal lumen. Ox forms more soluble complexes with other cations and results in HOx. Similar mechanisms may cause HOx following bariatric surgery. PHs are the most severe causes of HOx. Three types have so far been described, all being autosomic recessive. PH1 is due to mutations of AGXT gene encoding liver alanine-glyoxylate aminotransferase, PH2 is caused by mutations of GR-HPR gene encoding glyoxylate reductase and PH3 by mutations of HOGA1 encoding for hydroxyl-oxoglutarate aldolase. HOx results from deficient detoxification from glyoxylate, which is oxidized to Ox. The three PHs have different severity, though not always clinically distinguishable. They are identified through genetics and, in PH1, good genotype/phenotype correlations have been established. Thanks to early biochemical and genetic diagnosis, which are crucial to either prevent progression to ESRF or choose adequate transplantation strategies, the outlook of PH patients has dramatically improved in the last decades and will furtherly do in view of new therapeutic strategies.
Oxalate Content of Enteral Nutrition Formulas. [2020]Patients requiring oral and/or enteral nutrition support, delivered via nasogastric, gastric, or intestinal routes, have a relatively high incidence of calcium oxalate (CaOx) kidney stones. Nutrition formulas are frequently made from corn and/or or soy, both of which contain ample oxalate. Excessive oxalate intake contributes to hyperoxaluria (>45 mg urine oxalate/day) and CaOx stones especially when unopposed by concomitant calcium intake, gastrointestinal malabsorption is present, and/or oxalate degrading gut bacteria are limiting or absent. Our objective was to assess the oxalate content of commonly used commercial enteral nutrition formulas.
Prospective Randomized Evaluation of Idiopathic Hyperoxaluria Treatments. [2022]Purpose: Calcium oxalate (CaOx) stone formation is influenced by urinary oxalate excretion. Stone formers with elevated urinary oxalate are commonly prescribed a low-oxalate diet or oral supplementation with vitamin B6 and magnesium to reduce urinary oxalate excretion. This study aims to compare the effects of dietary modification vs supplementation vs a combination of both on urinary oxalate. Materials and Methods: We enrolled patients with a documented history of CaOx stones and newly diagnosed idiopathic hyperoxaluria. Patients were randomized into three treatment groups: low oxalate diet (D), supplementation with 25 mg vitamin B6 and 400 mg magnesium oxide (S), or both low oxalate diet and B6/magnesium supplementation (DS). Baseline and 3-month postintervention 24-hour urine tests were obtained. The primary endpoint was change in 24-hour urinary oxalate (Ox24) at 12 weeks. Secondary endpoints included changes in other 24-hour urine parameters, compliance rates, and adverse effect rates. Results: In total, 164 patients were recruited and 62, 47, and 55 were enrolled into the D, S, and DS groups, respectively. Of these, 99 patients completed the study (56.5% of the D, 72.3% of the S, and 54.6% of the DS groups, respectively). Significant differences were noted in median percent reduction in Ox24 values (-31.1% vs -16.0% vs -23.9%, p = 0.007) in the D, S, and DS groups, respectively. Furthermore, the percentages of patients within each treatment arm who realized a decrease in Ox24 were also found to be significantly different: D = 91.4% vs. S = 67.6% vs DS = 86.7%, p = 0.027. No significant adverse events were observed in any of the study arms. Conclusion: Low oxalate diet is more effective than B6/magnesium supplementation at lowering urinary oxalate in idiopathic hyperoxaluric stone formers. Combination therapy did not produce greater reductions in urinary oxalate than either of the monotherapy arms suggesting it is of little clinical utility. Further study with long-term longitudinal follow-up is required to determine if these treatment strategies reduce recurrent stone events in this population.
What treatments reduce kidney stone risk in patients with bowel disease? [2023]We examined how physicians made therapeutic choices to decrease stone risk in patients with bowel disease without colon resection, many of whom have enteric hyperoxaluria (EH), at a single clinic. We analyzed clinic records and 24-h urine collections before and after the first clinic visit, among 100 stone formers with bowel disease. We used multivariate linear regression and t tests to compare effects of fluid intake, alkali supplementation, and oxalate-focused interventions on urine characteristics. Patients advised to increase fluid intake had lower initial urine volumes (L/day; 1.3 ± 0.5 vs. 1.7 ± 0.7) and increased volume more than those not so advised (0.7 ± 0.6 vs. 0.3 ± 0.6 p = 0.03; intervention vs. non-intervention). Calcium oxalate supersaturation (CaOx SS) fell (95% CI -4.3 to -0.8). Alkali supplementation increased urine pH (0.34 ± 0.53 vs. 0.22 ± 0.55, p = 0.26) and urine citrate (mg/d; 83 ± 256 vs. 98 ± 166, p = 0.74). Patients advised to reduce oxalate (mg/day) absorption had higher urine oxalate at baseline (88 ± 44 vs. 50 ± 26) which was unchanged on follow-up (88 (baseline) vs. 91 (follow-up), p = 0.90). Neither alkali (95% CI -1.4 to 2.1) nor oxalate-focused advice (95% CI -1.2 to 2.3) lowered CaOx SS. Physicians chose treatments based on baseline urine characteristics. Advice to increase fluid intake increased urine volume and decreased CaOx SS. Alkali and oxalate interventions were ineffective.