CLINICAL TRIALS PROFILE FOR ANGIOTENSIN II ACETATE
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All Clinical Trials for angiotensin ii acetate
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00239096 ↗ | Prevention of Decompensation in Liver Cirrhosis | Unknown status | Else Poulsen Mindelegat | Phase 4 | 2005-09-01 | The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic. |
| NCT00239096 ↗ | Prevention of Decompensation in Liver Cirrhosis | Unknown status | Lundbeck Foundation | Phase 4 | 2005-09-01 | The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic. |
| NCT00239096 ↗ | Prevention of Decompensation in Liver Cirrhosis | Unknown status | University of Southern Denmark | Phase 4 | 2005-09-01 | The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic. |
| NCT00239096 ↗ | Prevention of Decompensation in Liver Cirrhosis | Unknown status | Odense University Hospital | Phase 4 | 2005-09-01 | The purpose of this study is to determine whether losartan, an angiotensin II blocker prevents the sodium retention in patients with liver cirrhosis and by that reduces the fluid retention. Moreover is the purpose to asses whether losartan is antifibrotic. |
| NCT00364000 ↗ | Arterial Stiffness and Calcifications in Haemodialysis Patients on Sevelamer or Calcium Acetate | Withdrawn | Romanian Society of Nephrology | N/A | 2012-01-01 | End-stage renal disease (ESRD) is a state of increased arterial stiffness of extensive vessel calcifications, compared with the non-renal population. Both arterial stiffness and arterial calcifications are potent predictors of all-cause and cardiovascular mortality in ESRD patients. Several studies have documented the direct relationship between the extent and severity of arterial/coronary calcifications and outcome in dialysis patients. The relationship is strong no matter if arterial calcifications were quantified by electron-beam computed tomography or a radiological calcification score. Calcifications are early and progressive events in these patients. PWV is strongly related to the degree of sonographic determined arterial calcifications and EBCT-derived coronary artery calcium score in chronic kidney disease patients. Calcium-based phosphate binders are associated with progressive coronary artery and aortic calcification, especially when mineral metabolism is not well controlled. According to recent studies, sevelamer hydrochloride is a potent non-calcium-containing phosphate binder, well tolerated in ESRD. Compared with calcium-based phosphate binders, sevelamer is less likely to cause hypercalcemia, low levels of PTH, and progressive coronary and aortic calcification in hemodialysis patients. Moreover, sevelamer has a favorable effect on the lipid profile. Less is known about the relationship between sevelamer treatment and progression of arterial stiffness. To date, there is one single study examining the influence of sevelamer (versus calcium carbonate) on the evolution of arterial stiffness in a very small number (N=15) of haemodialysis patients. These study used the same patients as historical controls, thus being methodologically rather weak. Moreover, the follow-up was quite short - 6 month. The aim of the trial is to to quantify, in a randomized opened-labeled controlled trial the effect of sevelamer hydrochloride on the evolution of arterial stiffness parameters (pulse wave velocity and the augmentation index) in chronic haemodialysis patients and to correlate these parameters with arterial calcification assessed by a previous described radiological score of arterial calcification and echocardiographic parameters (left ventricular hypertrophy, LV dilatation, systolic and diastolic dysfunction). |
| NCT00486772 ↗ | Sevelamer, Fetuin-A and Endothelial Dysfunction in CKD | Completed | Gulhane School of Medicine | Phase 4 | 1969-12-31 | Vascular calcification and endothelial dysfunction (ED) contribute to the development of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). Sevelamer, a non-calcium based phosphate binder, has been shown to attenuate cardiovascular calcification in CKD patients while the exact mechanism has not been clarified. This study was designed to investigate the effect of short-term sevelamer treatment on both serum fetuin-A concentrations and ED seen in CKD patients. |
| NCT01135615 ↗ | Sevelamer, FGF-23 and Endothelial Dysfunction in Chronic Kidney Disease (CKD) | Completed | Gulhane School of Medicine | Phase 4 | 2008-01-01 | Vascular calcification and endothelial dysfunction (ED) contribute to the development of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). Sevelamer, a non-calcium based phosphate binder, has been shown to attenuate cardiovascular calcification in CKD patients while the exact mechanism has not been clarified. This study was designed to investigate the effect of short-term sevelamer treatment on both serum FGF23 levels concentrations and ED seen in CKD patients. The researchers investigated the relationship between plasma FGF23 levels and the forearm blood flow response to ischemia in the forearm in a sizable series of incident stage 3-4 CKD patients. |
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