The VEGF and Diabetic Nephropathy
Take home points from Fuad Ziyadeh lecture
1. Glucose, glycosalation, ROS, TGF B and Ang II all increase VEGF –A ( in podocyte) and lead to proteinuria.
2. Two new players that might be interesting are Notch 1 and Mir 93 in this concept
3. Two mechanisms of albuminuria are paracrine and autocrine effects. Paracrine meaning effecting the receptor of the VEGF ad autocrine meaning affect the VEGF directly
4. Paracrine: increase glucose, ROS and ang II lead to endothelial NOS and VEGF expression and then vascular injury
5. Autocrine effects: a decrease in nephrin and nephrin is in the podocytes hence leading to an autocrine effects
6. A recent paper referenced below showed that VEGF was activated in many human GNs
7. Early in DM – you get increase VEGF, later on there is loss of podocytes and hence a decrease in VEGF. So using VEGF inhibitors can lead to bad outcomes as well and sclerosis.
Friday, November 19, 2010
ASN Live Update 2010: VEGF and Diabetic Nephropathy
Posted by Kenar D Jhaveri( kidney 007) at 12:00 PM
Labels: glomerular diseases, presentations
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