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- July 20, 2008 |
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"Interaction of Metabolic with Haemodynamic Factors in Diabetic Nephropathy"Prof. Mark E. Cooper (biography)
English - 2006-02-16 - 40 minutes
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Summary :
In this presentation Prof. Cooper discusses the pathogenesis of diabetic nephropathy, current treatments, and future directions for the development of new and better treatments.
Elevated glucose and blood pressure levels are both associated with the development of diabetic complications, as seen in the UKPD study. With regards to the pathogenesis of diabetic nephropathy, there seems to be an interaction between metabolic and haemodynamic factors to activate important pathways in the kidney, including the activation of growth factors and cytokines (1).
Blockade of the renin-angiotensin system is the currently the main treatment for diabetic nephropathy. Several studies have shown ACE inhibitor use to be associated with a reduction in urinary albumin excretion in even normotensive type 1 diabetic patients with microalbuminuria, and the RENAAL study further showed significant renal benefits due to treatment with the angiotensin-II-receptor antagonist losartan in type 2 diabetic patients with nephropathy (2). In the same study it was possible to look at baseline proteinuria and the antiproteinuric response to losartan in relation to renal outcomes (3). Prof. Cooper also discusses findings from the IDNT, IRMA 2 and CALM studies.
An example of a glucose-dependent pathway contributing to renal disease is the formation of advanced glycation end-products (AGEs). Prof. Cooper talks about the importance of tightening glycemic control, smoking cessation and reduction of dietary AGEs to reduce their harmful effects. Several agents have been shown experimentally to reduce AGE formation or cleave pre-formed AGEs.
Are there any newly discovered mechanisms by which antiproteinuric agents might be working? Prof. Cooper introduces "nephrin", a protein found between the glomerular epithelial cells. Nephrin expression was found to be reduced in diabetic patients with proteinuria, and there is evidence to suggest that glycated albumin and angiotensin II contribute to nephrin downregulation (4). Based on recent findings Prof. Cooper concludes with some possible future directions for the optimal treatment of diabetic nephropathy.
Copyright © 2006 E-MedHosting.com Inc.
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- A paradigm for the pathogenesis of diabetic nephropathy
- Efficacy of currently used antiproteinuric therapies and predictors of renal outcomes
- Potential therapeutic targets in diabetic nephropathy
Bibliographic references :
1. M. E. Cooper.Interaction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy Diabetologia, Volume 44, Issue 11, Nov 2001, Pages 1957 - 1972.
2. Barry M. Brenner, M.D., Mark E. Cooper, M.D., Ph.D., Dick de Zeeuw, M.D., Ph.D., William F. Keane, M.D., William E. Mitch, M.D., Hans-Henrik Parving, M.D., Giuseppe Remuzzi, M.D., Steven M. Snapinn, Ph.D., Zhonxin Zhang, Ph.D., Shahnaz Shahinfar, M.D., for the RENAAL Study Investigators. Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy N Engl J Med. 2001 Sep 20;345(12):861-9.
3. de Zeeuw D, Remuzzi G, Parving HH, Keane WF, Zhang Z, Shahinfar S, Snapinn S, Cooper ME, Mitch WE, Brenner BM.Proteinuria, a target for renoprotection in patients with type 2 diabetic nephropathy: Lessons from RENAAL Kidney International (2004) 65, 2309–2320.
4. Doublier S, Salvidio G, Lupia E, Ruotsalainen V, Verzola D, Deferrari G, Camussi G.Nephrin Expression Is Reduced in Human Diabetic Nephropathy: Evidence for a Distinct Role for Glycated Albumin and Angiotensin II Diabetes 52:1023-1030, 2003.
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