Preserved antioxidative defense of lipoproteins in renal failure and during hemodialysis

• Published in: American journal of kidney diseases Vol. 25; no. 4; p. 564
• Main Authors: Schulz, T, Schiffl, H, Scheithe, R, Hrboticky, N, Lorenz, R
• Format: Journal Article
• Language: English
• Published: United States 01.04.1995
• Subjects: Arteriosclerosis - etiology; Copper - pharmacology; Female; Humans; Kidney Failure, Chronic - metabolism; Kidney Failure, Chronic - therapy; Lipoproteins - metabolism; Lipoproteins, HDL - metabolism; Lipoproteins, LDL - metabolism; Male; Middle Aged; Oxidation-Reduction; Renal Dialysis
• ISSN: 0272-6386
• DOI: 10.1016/0272-6386(95)90124-8

Contact to artificial surfaces during hemodialysis activates leukocytes, which then form oxidized arachidonic acid products and free radicals. This might promote the oxidative modification of low-density lipoproteins (LDL) that play a key role in the initiation of atherosclerosis. Thus, leukocyte activation could specifically contribute to the high mortality from atherosclerotic complications on long-term hemodialysis. Therefore monitored LDL and high-density lipoprotein (HDL) resistance to copper-stimulated oxidation in patients with end-stage renal disease on maintenance hemodialysis with cellulose acetate or polysulfone membranes (n = 12), in patients with chronic renal failure (n = 13) and in healthy controls (n = 12). Six of the dialysis patients were restudied during a single cuprophane dialysis. Circulating leukocytes were reversibly reduced early in hemodialysis with cellulose acetate (minimum, 83.6% +/- 7.4% of baseline values at 30 minutes after dialysis start), polysulfone (minimum, 80.4% +/- 10.5% at 15 minutes; P < 0.05) and cuprophane (minimum, 24.5% +/- 8.5% at 60 minutes; P < 0.0001). Despite the leukocyte activation, LDL oxidation lag time was not shortened in comparison with healthy controls and was even prolonged at the end of cellulose acetate (P < 0.05) and cuprophane (P < 0.05) dialysis. HDL oxidation lag time increased (12.6% +/- 0.9%; P < 0.0001) 15 to 60 minutes after start of hemodialysis and returned to predialysis values thereafter. In patients with chronic renal failure, the lag time of HDL oxidation was significantly prolonged (13.34 minutes +/- 0.9) compared with healthy controls (10.91 +/- 2.0 minutes; P < 0.01) as well as compared with the dialysis patients at baseline (9.9 minutes +/- 1.4; P < 0.01).