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Uric Acid Stones clinical trials

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NCT ID: NCT06335537 Not yet recruiting - Uric Acid Stones Clinical Trials

Impact of Sodium Bicarbonate on 24-hour Urine Parameters in Hypocitriuric and Uric Acid Stone Formers

Start date: May 2024
Phase: Phase 1
Study type: Interventional

The incidence of kidney stone disease continues to rise globally. Although the treatment of kidney stone disease has dramatically improved in recent years, surgical management remains invasive and expensive. Patients who develop kidney stones are at high risk of recurrence during their lifetime; therefore, prevention of stones should be a primary focus. Low levels of citrate and acidic urine are risk factors for the formation of kidney stones such as calcium oxalate and uric acid, respectively. Calcium oxalate stones are the predominant stone composition in the United States, accounting for over 2/3rds of stones. Citrate is a key inhibitor of calcium oxalate crystal formation and thus increasing it in the urine of a calcium oxalate stone former is quite beneficial. Uric acid stones account for approximately 10 percent of all stone types. These stones form primarily due to an acidic urinary environment which is a prerequisite for crystal formation. Common medications for stone formers include potassium citrate which help to make the urine more alkaline. Although effective, these medications have side effects and may prove to be too expensive (upwards of $450/month). Consuming baking soda (sodium bicarbonate) may prove to be an inexpensive ($0.34/month) equally effective alternative with respect to increasing urinary citrate levels and alkalinizing the urine. Investigators hypothesize that twice a day oral baking soda in a liquid medium (e.g., water, orange juice, soda, etc.) can be an effective, and inexpensive alternative to urocit K with regard to alkalinizing the urine and raising urinary citrate levels.

NCT ID: NCT06118320 Recruiting - Uric Acid Stones Clinical Trials

The Effective of Potassium Sodium Hydrogen Citrate in Treating Uric Acid Stones Using Gut Microbiota and Metabolomics.

Start date: March 1, 2022
Phase:
Study type: Observational

The goal of this observational study is to investigate the alterations in gut microbiota and metabolites among patients with uric acid stones following the administration of potassium sodium hydrogen citrate. The main question it aims to predict the potential metabolic mechanism and therapeutic target of potassium sodium hydrogen citrate in treating uric acid stones through analysis of gut microbiota and metabolomics. The participants were required to undergo a 3-month drug intervention, providing blood, urine, and stool samples before and after treatment. No additional interventions were implemented for the subjects.

NCT ID: NCT04621929 Recruiting - Obesity Clinical Trials

Obesity and Uric Acid Stones Study

Start date: March 31, 2021
Phase: Phase 3
Study type: Interventional

The investigator proposes an 18 month, feasibility pilot study, randomizing obese and diabetic individuals with pure uric acid nephrolithiasis (UAN) or mixed calcium oxalate (CO) UAN to either phentermine/topiramate or a pragmatic control group who will remain on their standard medication regimen (citrate salts, allopurinol, diet, etc.).

NCT ID: NCT04352153 Recruiting - Hyperuricemia Clinical Trials

Role of Uralyt-U in Patients With Hyperuricemia

Start date: April 1, 2020
Phase: N/A
Study type: Interventional

The purpose of the study is to provide a more direct and objective basis for the widespread use of potassium sodium hydrogen citrate granules in the treatment of uric acid stones.

NCT ID: NCT02561858 Completed - Uric Acid Stones Clinical Trials

Toxicity of Perirenal Fat in Overweight or Obese Subjects: A Pathophysiological Link Between Uric Acid Stones and Renal Ammonium Formation

Start date: October 14, 2015
Phase: N/A
Study type: Interventional

Patients who are overweight or obese, diabetic or not, share with those who are suffering from uric stones the same way to remove abnormal acidity of the body in urine, ie a kidney ammoniogenesis default. This results in an overly acidic urine pH which is directly pathogenic in people predisposed to develop uric stones because the precipitation of urate soluble uric acid is accelerated in acid medium. Excess visceral fat, particularly perirenal, this defect may promote formation of renal ammonium. Indeed, the perirenal fat is adjacent to the renal cortex and shares with it a common arterial supply via the plexus Turner. Adipokines and fatty acids of the perirenal fat are predisposed to gain the renal cortex, seat of the ammoniogenesis. In humans the pathogenic role of the perirenal fat is demonstrated in chronic kidney disease and essential hypertension. However, the amount of fat and perirenal that of intra-abdominal fat are positively correlated. Investigators hypothesis is that the perirenal fat also exert a pathogenic role in uric because of anatomical links between kidney stones and greasy environment and because excess fatty acids reaching the renal cortex decreases ammoniogenesis in an animal model metabolic syndrome. For the test, the investigators will compare the amount of fat and perirenal renal ability to form ammonium in patients with uric or calcium lithiasis taking into account the amount of intra-abdominal fat.