PMID- 11158876
OWN - NLM
STAT- MEDLINE
DCOM- 20010426
LR  - 20190815
IS  - 1523-6838 (Electronic)
IS  - 0272-6386 (Linking)
VI  - 37
IP  - 1 Suppl 2
DP  - 2001 Jan
TI  - Proteinuria and plasma compositional changes contribute to defective lipoprotein 
      catabolism in the nephrotic syndrome by separate mechanisms.
PG  - S119-22
AB  - Triglyceride (TG)-rich lipoproteins are primarily increased in the nephrotic 
      syndrome (NS) as a result of decreased catabolism. Lipoprotein lipase (LpL) is 
      the rate limiting enzyme for lipolysis of TG. The biologically active endothelial 
      bound LpL pool is reduced in NS providing one mechanism for decreased clearance 
      of very low density lipoprotein (VLDL). LpL, however, is also reduced in the 
      Nagase Analbuminemic Rat (NAR) to the same extent as in NS, suggesting that other 
      factors contribute to decreased VLDL clearance. Hyperlipidemia worsens with the 
      onset of proteinuria and is reduced when proteinuria abates. We established that 
      while VLDL from NS rats bind poorly to bovine aortic endothelial cells (BAEC) in 
      the presence of saturating LpL while, VLDL from NAR bind more avidly than 
      control. We then established that rat aortic endothelial cells (RAEC) incubated 
      with serum from NAR or from NS rats bind significantly less exogenous LpL. Thus 
      decreased clearance of VLDL in NS results from: 1) reduced endothelial bound LpL; 
      an effect of serum from animals with reduced oncotic pressure (pi) that makes 
      cells unable to bind LpL; and 2) an alteration in VLDL binding to endothelial 
      bound LpL. The former has no relationship to proteinuria while the latter occurs 
      as a consequence of proteinuria. These effects combine to suppress VLDL 
      clearance.
FAU - Shearer, G C
AU  - Shearer GC
AD  - Division of Nephrology, Department of Medicine, University of California Davis, 
      Davis, USA.
FAU - Kaysen, G A
AU  - Kaysen GA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Am J Kidney Dis
JT  - American journal of kidney diseases : the official journal of the National Kidney 
      Foundation
JID - 8110075
RN  - 0 (Culture Media)
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (Lipids)
RN  - 0 (Lipoproteins)
RN  - 0 (Lipoproteins, VLDL)
RN  - 0 (Serum Albumin)
RN  - EC 3.1.1.34 (Lipoprotein Lipase)
SB  - IM
MH  - Animals
MH  - Binding, Competitive/drug effects
MH  - Cattle
MH  - Cells, Cultured
MH  - Culture Media/pharmacology
MH  - Endothelium, Vascular/cytology/metabolism
MH  - Iodine Radioisotopes
MH  - Lipids/*blood
MH  - Lipoprotein Lipase/metabolism
MH  - Lipoproteins/*metabolism
MH  - Lipoproteins, VLDL/metabolism
MH  - Male
MH  - Nephrotic Syndrome/*metabolism
MH  - Protein Binding
MH  - Proteinuria/*physiopathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Serum Albumin/metabolism
EDAT- 2001/02/13 11:00
MHDA- 2001/05/11 10:01
CRDT- 2001/02/13 11:00
PHST- 2001/02/13 11:00 [pubmed]
PHST- 2001/05/11 10:01 [medline]
PHST- 2001/02/13 11:00 [entrez]
AID - S0272-6386(01)35561-0 [pii]
AID - 10.1053/ajkd.2001.20766 [doi]
PST - ppublish
SO  - Am J Kidney Dis. 2001 Jan;37(1 Suppl 2):S119-22. doi: 10.1053/ajkd.2001.20766.