The Effects of Decreasing the Lasix Dose on the Cardiorenal System
This trial is active, not recruiting.
|Conditions||heart failure, kidney dysfunction|
|Phase||phase 1/phase 2|
|Collaborator||National Institutes of Health (NIH)|
|Start date||July 2009|
|End date||July 2014|
|Trial size||36 participants|
|Trial identifier||NCT00982423, 09-003210, 1RO1HL84155-01A2 Aim 1|
The investigators' objective is to define the effects of decreasing the furosemide dose on heart, kidney and humoral function in people with compensated heart failure and kidney dysfunction and also in people with compensated heart failure without kidney dysfunction. Secondly, to define the humoral activation in both groups.
|Endpoint classification||safety/efficacy study|
|Intervention model||single group assignment|
The primary endpoint will to define from baseline after 3 weeks of decreasing the furosemide dose change of GFR, effective renal plasma flow (ERPF) and Aldosterone within the compensated CHF with renal dysfunction, and within the compensated
time frame: 3 years
The secondary endpoints include: 1)determine differences in activation of RAAS, assessed plasma renin, angiotensin and aldosterone and renal cGMP generation in subjects with compensated CHF and renal dysfunction and those with compensated C
time frame: 3 years
Male or female participants from 18 years up to 90 years old.
- Left ventricular ejection fraction of equal or less than 40%assessed echocardiography, nuclear scan or left ventriculogram within the past 36 months.
- Stable New York Heart Association (NYHA) class II and III symptoms as defined by; a) no change in NYHA symptoms over the past 3 months; b) on stable doses of ACE inhibitor or beta blocker or digoxin or furosemide or AT1 blocker over the past 3 months; c) no episode of decompensated CHF over the past 6 months.
- Calculated creatinine clearance of equal or less than 60 ml/min and greater than 20 ml/min, using the Cockcroft-Gault formula assessed within the past 36 months and a confirmatory calculated creatinine clearance equal or less than 60 ml/min and greater than 20 ml/min at the time of enrollment.
- Prior diagnosis of intrinsic renal diseases including renal artery stenosis of > 50%
- Peritoneal or hemodialysis within 90 days or anticipation that dialysis or ultrafiltration of any form will be required during the study period
- Patients who are taking aldosterone antagonist
- Hospitalization for decompensated CHF during the past 6 months
- Subjects on other diuretics besides furosemide.
- Myocardial infarction within 6 months of screening
- Unstable angina within 6 months of screening or any evidence of myocardial ischemia
- Significant valvular stenosis, hypertrophic, restrictive or obstructive cardiomyopathy, constrictive pericarditis, primary pulmonary hypertension, or biopsy proven active myocarditis
- Severe congenital heart diseases
- Sustained ventricular tachycardia or ventricular fibrillation within 14 days of screening
- Second or third degree heart block without a permanent cardiac pacemaker
- Stroke within 3 months of screening or other evidence of significantly compromised CNS perfusion
- Alanine Aminotransferase (ALT) result >1.5 times the upper limit of normal
- Serum sodium of < 125 mEq/dL or > 150 mEq/dL
- Serum potassium of < 3.5 mEq/dL or > 5.5 mEq/dL
- Serum digoxin level of > 2.0 ng/ml
- Hemoglobin < 10 gm/dl
- Other acute or chronic medical conditions or laboratory abnormality which may increase the risks associated with study participation or may interfere with interpretation of the data
- Received an investigational drug within 1 month prior to dosing
- Patients with an allergy to iodine.
- Female subject who is pregnant or breastfeeding
- In the opinion of the investigator is unlikely to comply with the study protocol or is unsuitable for any reasons
|Official title||To Define the Effects of Decreasing the Furosemide Dose on Cardiorenal and Humoral Function in Humans With Compensated CHF With and Without Renal Dysfunction|
|Principal investigator||Horng H Chen, MD|
|Description||The broad objective of this protocol is to advance our understanding of the pathophysiological mechanisms of human Cardiorenal Syndrome (CRS) with a specific emphasis upon the biological interaction between diuretic therapy, the renin-angiotensin-aldosterone-system (RAAS) and cyclic 3'-5'-guanosine monophosphate (cGMP) pathway.|
Call for more information