TITLE

Transvascular lipoprotein transport in patients with chronic renal disease

AUTHOR(S)
Jensen, Trine Krogsgaard; Nordestgaard, Borge Gronne; Feldt-Rasmussen, Bo; Jensen, Kurt Svarre; Jensen, Jan Skov
PUB. DATE
July 2004
SOURCE
Kidney International;Jul2004, Vol. 66 Issue 1, p275
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Transvascular lipoprotein transport in patients with chronic renal disease. Background. While increased plasma cholesterol is a well-established cardiovascular risk factor in the general population, this is not so among patients with chronic renal disease. We hypothesized that the transvascular lipoprotein transport, in addition to the lipoprotein concentration in plasma, determines the degree of atherosclerosis among patients with chronic renal disease. Methods. We used an in vivo method for measurement of transvascular transport of low-density lipoprotein (LDL) in 21 patients with chronic renal disease and in 42 healthy control patients. Autologous 131-iodinated LDL was reinjected intravenously, and the 1-hour fractional escape rate was taken as index of transvascular transport. Results. Transvascular LDL transport tended to be lower in patients with chronic renal disease than in healthy control patients [3.3 (95% CI 2.4–4.2) vs. 4.2 (3.7–4.2)%/hour; NS]. However, this tendency disappeared when transvascular LDL transport was corrected for distribution volume of LDL [1.7 (1.2–2.2) vs. 1.8 (1.6–2.0) %/(hour × (L/m2)); NS]. There was significant variation in transvascular LDL transport between diabetic patients with chronic renal disease, nondiabetic patients with chronic renal disease, and healthy control patients [5.0 (3.2–7.8) vs. 3.0 (2.2–3.8) vs. 4.2 (3.6–4.8) %/hour; P < 0.01 after adjustment for distribution volume of LDL]. This variation was unlikely caused by altered hepatic LDL receptor expression or glycosylation of LDL in diabetes patients. Conclusion. Transvascular LDL transport may be increased in diabetic patients with chronic renal disease, suggesting that lipoprotein flux into the arterial wall is increased. A similar mechanism does not operate in nondiabetic patients with chronic renal disease.
ACCESSION #
13347231

 

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