Abstract
The elevated glomerular filtration rate that occurs in 25 to 40 percent of insulin-dependent diabetics has been proposed as having a role in the initiation and evolution of diabetic nephropathy. We report that both enhanced NO synthesis by ecNOS in afferent arterioles and glomerular endothelial cells and increased expression of IGF-1 receptor can cause glomerular hyperfiltration, and that upregulated expression of ICAM-1 can promote the intraglomerular infiltration of mononuclear cells, which were prevented by aldose reductase inhibitor. The results of United Kingdom Prospective Diabetes Study (UKPDS) will also be discussed.
Original language | English |
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Pages (from-to) | 590-600 |
Number of pages | 11 |
Journal | Nippon rinsho. Japanese journal of clinical medicine |
Volume | 57 |
Issue number | 3 |
Publication status | Published - Mar 1999 |
ASJC Scopus subject areas
- Medicine(all)