CLINICAL TRIALS PROFILE FOR AMINOHIPPURATE SODIUM
✉ Email this page to a colleague
All Clinical Trials for AMINOHIPPURATE SODIUM
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00722215 ↗ | Endothelin Receptor Antagonism in Proteinuric Nephropathy | Completed | British Heart Foundation | Phase 1 | 2006-05-01 | The number of people with kidney problems is increasing rapidly, related in part to the increasing prevalence of diabetes. Patients with kidney problems tend to have protein leaking into the urine (proteinuria). Both proteinuria and the kidney disease itself are associated with an increased risk of heart disease. Reducing proteinuria is an important treatment goal in people with kidney problems. Endothelin is a chemical produced both by blood vessels and the kidney. Higher than normal levels of endothelin are thought to contribute to progression of kidney disease and proteinuria. By using drugs that block the effects of endothelin ('endothelin receptor antagonists') we can hopefully reduce both of these. The purpose of the study is to ascertain whether endothelin receptor antagonists improve kidney function and reduce proteinuria more so than other commonly used drugs. |
| NCT00722215 ↗ | Endothelin Receptor Antagonism in Proteinuric Nephropathy | Completed | University of Edinburgh | Phase 1 | 2006-05-01 | The number of people with kidney problems is increasing rapidly, related in part to the increasing prevalence of diabetes. Patients with kidney problems tend to have protein leaking into the urine (proteinuria). Both proteinuria and the kidney disease itself are associated with an increased risk of heart disease. Reducing proteinuria is an important treatment goal in people with kidney problems. Endothelin is a chemical produced both by blood vessels and the kidney. Higher than normal levels of endothelin are thought to contribute to progression of kidney disease and proteinuria. By using drugs that block the effects of endothelin ('endothelin receptor antagonists') we can hopefully reduce both of these. The purpose of the study is to ascertain whether endothelin receptor antagonists improve kidney function and reduce proteinuria more so than other commonly used drugs. |
| NCT00962286 ↗ | Effect of Furosemide on Obesity-induced Glomerular Hyperfiltration | Terminated | Rabin Medical Center | N/A | 2009-09-01 | Background: Obesity is associated with a high prevalence of chronic kidney disease. The glomerular hyperfiltration associated with obesity may play a role in the pathogenesis of obesity associated chronic kidney disease. Attenuation of hyperfiltration by pharmacological means may slow down the development and progression of chronic renal failure. The investigators have previously shown that acetazolamide, a proximally acting diuretic that activates TGF by increasing solute delivery to the macula densa, abates glomerular hyperfiltration. The present study was designed to test the hypothesis that this decrease in hyperfiltration is specific to acetazolamide and not due to a non specific diuretic effect. The aim of the present study is to evaluate the effects of the administration of furosemide p.o. to subjects with severe obesity on glomerular hemodynamics. Methods: Ten obese subjects will participate in the study. They will undergo measurement of glomerular filtration rate (inulin clearance) (GFR), renal plasma flow (RPF) (p-aminohippuric acid clearance), filtration fraction, fractional excretion of lithium (FE LI) and blood pressure, before and after administration of oral furosemide 20 to 40 mg bid for 3 days. The effects of furosemide on glomerular hemodynamics in obese subjects will be compared to the previously studied effects of acetazolamide. |
| NCT01146288 ↗ | Effect of Acetazolamide and Furosemide on Obesity-induced Glomerular Hyperfiltration | Completed | Rabin Medical Center | N/A | 2010-07-01 | Background: Obesity is associated with a high prevalence of chronic kidney disease.The glomerular hyperfiltration associated with obesity may play a role in the pathogenesis of obesity associated chronic kidney disease. Attenuation of hyperfiltration by pharmacological means may slow down the development and progression of chronic renal failure. The investigators have previously shown that acetazolamide, a proximally acting diuretic that activates tubuloglomerular feedback(TGF) by increasing solute delivery to the Macula DENSA, abates glomerular hyperfiltration. The present study was designed to test the hypothesis that this decrease in hyperfiltration is specific to acetazolamide and not due to a non specific diuretic effect. The aim of the present study is to compare the effects of furosemide and acetazolamide on glomerular hemodynamics in subjects with severe obesity. Methods: A randomized double-blind crossover controlled design will be used. Fifteen obese subjects and ten subjects with normal body weight will participate in the study. Obese subjects will undergo measurement of glomerular filtration rate (GFR)(inulin clearance), renal plasma flow (RPF) (p-aminohippuric acid clearance), filtration fraction, fractional excretion of lithium (FE LI) and blood pressure, before and after intravenous administration of furosemide 2 mg. and acetazolamide 5 mg/kg BW. Ten subjects with normal body weight will undergo measurement of renal function without administration of diuretics. |
| NCT01156220 ↗ | Investigation of Gender Specificity of the Effects of Furosemide in Healthy Female and Male Volunteers | Withdrawn | Universitätsklinikum Hamburg-Eppendorf | Phase 4 | 2012-01-01 | In this study the gender specificity of the effects of furosemide in female and male volunteers will be investigated. The main objective is gender-specific comparison of the pharmacokinetic parameters of furosemide in relation to the effect of furosemide (urinary excretion). Secondary objectives are the gender-specific comparison of renal and systemic PAH clearance with the clearance of furosemide and the influence of various genetic polymorphisms on the variability of furosemide pharmacokinetics. |
| NCT02631148 ↗ | Effects of Melatonin Supplementation on Renal Physiology in a Habitual Sleep Restricted Population. | Terminated | Brigham and Women's Hospital | Phase 2 | 2016-01-01 | In a 6 week pilot study, 20 individuals with habitual sleep restriction will all be asked to extend their nightly sleep by 1 hour, and will then be randomized 1:1 to nightly controlled-release oral melatonin (2mg) or placebo. The investigators will assess whether sleep extension and nightly melatonin supplementation in the community is a feasible intervention with a beneficial effect on the following chronic kidney disease (CKD) risk factors: systemic and renal specific renin-aldosterone-angiotensin system (RAAS) activation (systemic plasma renin activity, plasma angiotensin II levels, 24-hour urine aldosterone excretion, and renal plasma flow response to captopril); nocturnal blood pressure measured by 24-hour ambulatory blood pressure monitor; central blood pressure measured by pulse wave analysis; and glucose metabolism measured by Minimal Model assessment of insulin resistance and β-cell response to a mixed meal protocol. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
Clinical Trial Conditions for AMINOHIPPURATE SODIUM
Condition Name
Clinical Trial Locations for AMINOHIPPURATE SODIUM
Trials by Country
Clinical Trial Progress for AMINOHIPPURATE SODIUM
Clinical Trial Phase
Clinical Trial Sponsors for AMINOHIPPURATE SODIUM
Sponsor Name
