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Originally Posted by Hero This is true, but what is the mechanism? I have already highlighted the exact mechanism. Actually in renal artery stenosis, efferent arteriole constriction by angiotensin II maintains the glomerular filtration and ACE-I inbihits the conversion of AI to AII and thus glomerular filtration is reduced --renal failure occurs. That's why ACE-I is usually not used in renal artery stenosis.
But ACE-I is drug of choice in diabetic nephropathy. Why? |
To answer your question,Diabetic nephropathy is characterized by among other things, tubulointerstitial fibrosis.Its pathogenesis is mediated by a number of chemokines with MCP-1(monocyte chemoattractant protein)showing the highest association.It is known that AT-II(angiotensin II) induces the MCP-1 gene.It follows that inhibitors of AT-II would abrogate MCP-1 expression and therefore improve diabetic nephropathy.