Effect of XXXX on experimental @entity2316 .

@entity1 @entity8 @entity6 @entity2316 @entity1421 @entity117 @entity3839 @entity2918 @entity35 @entity1281
The decline in glomerular filtration rate (GFR) in long-term @entity6 in @entity1 and animals in preceded by a period of hyperfiltration that may be responsible for it. The mediators of the increase in glomerular filtration are unknown, but recent studies suggest a prominent role for @entity2918 . To test the hypothesis that prostaglandins mediate early hyperfiltration and contribute to the progression of @entity2316 , we examined the effects of long-term @entity117 (ASA) treatment on whole kidney GFR and renal @entity1421 ( @entity1421 ) synthesis in control and @entity6 @entity35 8 days and 16 weeks after @entity3839 administration. The @entity35 were divided into four groups, control, control with ASA (C/ASA), @entity6 , and @entity6 with ASA (D/ASA). We found that 8 days after @entity3839 treatment, @entity1421 synthesis and GFR were increased in @entity6 @entity35 . @entity1281 treatment inhibited renal prostaglandin synthesis and prevented the GFR increase. ASA given to control @entity35 reduced @entity1421 synthesis without changing GFR. In the 16-week study @entity6 @entity35 had lower GFR and increased renal @entity1421 synthesis. @entity6 @entity35 also had thickened @entity8 membrane compared with control @entity35 . By contrast GFR did not fall and thickening of the @entity8 membrane did not occur in @entity6 @entity35 receiving ASA. ASA had no effect on GFR or @entity8 membrane in normal @entity35 but decreased renal @entity1421 synthesis. The data demonstrate that @entity117 prevents early hyperfiltration and prevents the fall in GFR and @entity8 membrane thickening that occurs over time in @entity6 @entity35 . Inhibition of @entity1421 synthesis by @entity117 , or some other effect of @entity117 , may be responsible for the protection observed.
