Proteinuria and Plasma Compositional Changes Contribute to Defective Lipoprotein Catabolism in the Nephrotic Syndrome by Separate Mechanisms
作者： Gregory C. Shearer , George A. Kaysen
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摘要: Abstract Triglyceride (TG)-rich lipoproteins are primarily increased in the nephrotic syndrome (NS) as a result of decreased catabolism. Lipoprotein lipase (LpL) is rate limiting enzyme for lipolysis TG. The biologically active endothelial bound LpL pool reduced NS providing one mechanism clearance very low density lipoprotein (VLDL). LpL, however, also Nagase Analbuminemic Rat (NAR) to same extent NS, suggesting that other factors contribute VLDL clearance. Hyperlipidemia worsens with onset proteinuria and when abates. We established while from rats bind poorly bovine aortic cells (BAEC) presence saturating while, NAR more avidly than control. then rat (RAEC) incubated serum or significantly less exogenous LpL. Thus results from: 1) LpL; an effect animals oncotic pressure (π) makes unable 2) alteration binding former has no relationship latter occurs consequence proteinuria. These effects combine suppress
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