Ignite Creation Date:
2024-05-06 @ 12:39 AM
Last Modification Date:
2024-10-26 @ 10:52 AM
Study NCT ID:
NCT01624064
Status:
UNKNOWN
Last Update Posted:
2012-06-20
First Post:
2012-06-16
Brief Title:
Renal Effects of an Angiotensin Converting Enzyme Inhibitor in Adults With Chronic Kidney Disease of Uncertain Aetiology
Sponsor:
Ministry of Health Sri Lanka
Organization:
Ministry of Health Sri Lanka
Study Overview
Official Title:
A Double Blind Clinical Trial to Examine the Renal Effects of an Angiotensin Converting Enzyme Inhibitor Enalapril in Adults With Chronic Kidney Disease of Uncertain Aetiology CKDu
Status:
UNKNOWN
Status Verified Date:
2012-06
Last Known Status:
NOT_YET_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
CKDu
Brief Summary:
Enalapril would significantly reduce progression of renal disease in patients with Chronic Kidney Disease of Uncertain aetiology
Detailed Description:
End Stage Kidney Disease ESKD results in reduced life expectancy quality of life and increased consumption of health care resources Chronic Kidney Disease of Uncertain aetiology CKDu is being increasingly recognized in the North Central Region of Sri Lanka and in certain regions over 25 unpublished data of general population is suspected as suffering from CKDu The number of patients who reach ESKD that requires hemodialysis or transplantation is increasing highlighting the need to find strategies that slow progression of kidney disease The need for these strategies is even more critical in Sri Lanka where dialysis in not a preferred treatment option Treatment strategies should be readily accessible and cheap
The importance of proteinuria as a significant risk factor for ESKD is well recognized and treatment that is targeted at reducing proteinuria has been shown to reduce progression of renal disease The Renin - Angiotensin - Aldosterone - System RAAS is directly involved in the regulation of blood pressure fluid volume and vascular response to injury and inflammation The inappropriate activation of this system causes hypertension fluid retention and inflammatory thrombotic and atherogenic effects that may contribute to end-organ damage in the long term Angiotensin II mediates hemodynamic effects as well as inflammation and fibrosis in the kidney heart and vasculature
Numerous clinical trials have established that interruption of the RAAS cascade with angiotensin-converting enzyme inhibitors ACEI or angiotensin receptor blockers ARB is beneficial in slowing progression of renal disease Reduction of BP lowers proteinuria but the use of an ACEI or an ARB reduces both proteinuria and the rate of deterioration of renal function beyond those seen with equivalent BP reduction from conventional antihypertensive agents However the use of these agents has limitations with significant numbers of treated patients still demonstrating progressive renal disease RAAS blockers have been shown to blunt the progression of advanced kidney disease However the long-term renal effect of these agents in early renal disease is not well demonstrated In fact the trials which showed benefits with RAAS blockers did show in glomerular disease and evidence is not so strong in tubulo-interstitial disease The benefits of RAS inhibition seem to depend on the degree of proteinuria at baseline It is marginal in those with low grade proteinuria
In most forms of proteinuric chronic renal disease glomerular filtration rate continues to decline even when the initial insult has been removed The cause of CKDu is still unknown CKDu is a tubulo-interstitial disease with low grade proteinuria We believe that the place of ACEI for secondary prevention of CKDu progression needs investigation
The importance of proteinuria as a significant risk factor for ESKD is well recognized and treatment that is targeted at reducing proteinuria has been shown to reduce progression of renal disease The Renin - Angiotensin - Aldosterone - System RAAS is directly involved in the regulation of blood pressure fluid volume and vascular response to injury and inflammation The inappropriate activation of this system causes hypertension fluid retention and inflammatory thrombotic and atherogenic effects that may contribute to end-organ damage in the long term Angiotensin II mediates hemodynamic effects as well as inflammation and fibrosis in the kidney heart and vasculature
Numerous clinical trials have established that interruption of the RAAS cascade with angiotensin-converting enzyme inhibitors ACEI or angiotensin receptor blockers ARB is beneficial in slowing progression of renal disease Reduction of BP lowers proteinuria but the use of an ACEI or an ARB reduces both proteinuria and the rate of deterioration of renal function beyond those seen with equivalent BP reduction from conventional antihypertensive agents However the use of these agents has limitations with significant numbers of treated patients still demonstrating progressive renal disease RAAS blockers have been shown to blunt the progression of advanced kidney disease However the long-term renal effect of these agents in early renal disease is not well demonstrated In fact the trials which showed benefits with RAAS blockers did show in glomerular disease and evidence is not so strong in tubulo-interstitial disease The benefits of RAS inhibition seem to depend on the degree of proteinuria at baseline It is marginal in those with low grade proteinuria
In most forms of proteinuric chronic renal disease glomerular filtration rate continues to decline even when the initial insult has been removed The cause of CKDu is still unknown CKDu is a tubulo-interstitial disease with low grade proteinuria We believe that the place of ACEI for secondary prevention of CKDu progression needs investigation
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None