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Generated: July 17, 2019

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CLINICAL TRIALS PROFILE FOR ANGIOTENSIN II ACETATE

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Clinical Trials for angiotensin ii acetate

Trial ID Title Status Sponsor Phase Summary
NCT00239096 Prevention of Decompensation in Liver Cirrhosis Unknown status Else Poulsen Mindelegat Phase 4 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 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 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 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 Unknown status Romanian Society of Nephrology N/A 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).
Trial ID Title Status Sponsor Phase Summary

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Clinical Trial Conditions for angiotensin ii acetate

Condition Name

Condition Name for angiotensin ii acetate
Intervention Trials
Hyperphosphatemia 1
Haemodialyzed Patients 1
Cough 1
Ascites 1
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Condition MeSH

Condition MeSH for angiotensin ii acetate
Intervention Trials
Calcinosis 1
Liver Cirrhosis, Alcoholic 1
Liver Cirrhosis 1
Fibrosis 1
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Clinical Trial Locations for angiotensin ii acetate

Trials by Country

Trials by Country for angiotensin ii acetate
Location Trials
United States 3
Turkey 1
Romania 1
Denmark 1
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Trials by US State

Trials by US State for angiotensin ii acetate
Location Trials
North Carolina 1
New York 1
Colorado 1
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Clinical Trial Progress for angiotensin ii acetate

Clinical Trial Phase

Clinical Trial Phase for angiotensin ii acetate
Clinical Trial Phase Trials
Phase 4 3
Phase 2 1
N/A 1
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Clinical Trial Status

Clinical Trial Status for angiotensin ii acetate
Clinical Trial Phase Trials
Unknown status 2
Completed 2
Not yet recruiting 1
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Clinical Trial Sponsors for angiotensin ii acetate

Sponsor Name

Sponsor Name for angiotensin ii acetate
Sponsor Trials
Gulhane School of Medicine 2
Romanian Society of Nephrology 1
Odense University Hospital 1
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Sponsor Type

Sponsor Type for angiotensin ii acetate
Sponsor Trials
Other 9
NIH 1
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