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Dual RAS-blockade by ACE-inhibition and AT1 receptor blockade, role of the ACE I/D genotype and low sodium diet in non-diabetic proteinuric patients.


- candidate number2082
- NTR NumberNTR675
- ISRCTNISRCTN50137410
- Date ISRCTN created29-jun-2006
- date ISRCTN requested13-jun-2006
- Date Registered NTR5-mei-2006
- Secondary IDsN/A 
- Public TitleDual RAS-blockade by ACE-inhibition and AT1 receptor blockade, role of the ACE I/D genotype and low sodium diet in non-diabetic proteinuric patients.
- Scientific TitleDual RAS-blockade by ACE-inhibition and AT1 receptor blockade, role of the ACE I/D genotype and low sodium diet in non-diabetic proteinuric patients- a double blind randomised, plcebo controlled cross-over trial.
- ACRONYMDUAAAL
- hypothesisThe recently found gene-environment interaction between dietary sodium intake and the ACE genotype with sodium-induced therapy resistance to ACE inhibition in DD homozygotes (that was absent in II and ID subjects) is present in the renal patient as well. With regard to the pathophysiological mechanism, we hypothesise that a high dietary sodium intake induces an increase in tissue ACE activity, which is stronger in the DD homozygotes, resulting in a worse therapy response to ACEi. The alleged sodium-induced therapy resistance of the DD homozygotes may therefore be overcome by addition of AT1 receptor blockade, since AT1 receptor blockers act “downstream” of the ACE. Moreover, we hypothesize that low dietary sodium intake has additional effects on proteinuria and blood pressure on top of dual RAS blockade in patients with non-diabetic proteinuria.
- Healt Condition(s) or Problem(s) studiedProteinuria
- Inclusion criteria1. Age older than 18 year; 2. Chronic non-diabetic renal disease, as established by history, urine analysis, serum biochemistry tests and/or renal biopsy; 3. Creatinine clearance > 30 ml/min/1.73 m; 4. Residual proteinuria > 1 g/24h.
- Exclusion criteria1. Failure to comply with the above inclusion criteria; 2. Diabetes mellitus; 3. Any contra-indication against the use of ACE inhibitors or AT1 receptor blockers; 4. A history of myocardial infarction, unstable angina, coronary by-pass or CVA during the past 6 months; 5. Heart failure NYHA class III-IV; 6. High rate of renal function loss (decline in creatinine clearance > 6 ml/min/1.73m2 during the previous year); 7. Need for treatment with corticosteroids, NSAID’s or immunosuppressive drugs; 8. Proteinuria > 10 g/24h and hypoalbuminaemia < 28 g/L; 9. Renovascular hypertension, malignant hypertension (diastolic blood pressure > 100 mmHg); 10. Serum potassium > 6 mmol/L.
- mec approval receivedyes
- multicenter trialyes
- randomisedyes
- masking/blindingDouble
- controlPlacebo
- groupCrossover
- Type-
- Studytypeintervention
- planned startdate 28-apr-2006
- planned closingdate1-sep-2008
- Target number of participants56
- InterventionsLisinopril 40 mg, with the addition of valsartan 320 mg (160 mg 1dd2) or placebo, both during low dietary sodium intake and high dietary sodium intake in randomised order.
- Primary outcomeThe primary endpoint will be reduction of proteinuria and blood pressure expressed as percentage change from baseline and analysed with each patient as his or her own control.
- Secondary outcome1. Serum creatinine; 2. Circulating RAS parameters; 3. Lipid profile; 4. Adiponectin.
- Timepoints
- Trial web siteN/A
- statusopen: patient inclusion
- CONTACT FOR PUBLIC QUERIESDrs. F. Waanders
- CONTACT for SCIENTIFIC QUERIESDrs. F. Waanders
- Sponsor/Initiator University Medical Center Groningen (UMCG), Novartis Pharma AG
- Funding
(Source(s) of Monetary or Material Support)
Novartis Pharma B.V.
- PublicationsN/A
- Brief summaryThe DUAAAL study is a double blind, randomized, crossover study to study whether the gene environment interaction between the ACE genotype, dietary sodium intake and the response to ACE inhibition which is present in healthy subjects, is also present in a clinically relevant setting, in renal patients. Moreover, we study if this assumed therapy resistance in the DD genotype, could be overcome by the addition of an ARB and whether this assumed additional effect is dependent on the genotype and dietary sodium intake. 56 patients with a stable non-diabetic proteinuria will be included, who will, after a run-in period of 6 weeks where lisonopril 40 mg will be prescribed, treated with either placebo or valsartan 320 mg (160 mg 1dd2)for 6 weeks on top of their ACEi treatment in randomized order on both a low and a high sodium diet.
- Main changes (audit trail)
- RECORD5-mei-2006 - 3-jul-2006


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