PRESERVED ANTIOXIDATIVE DEFENSE OF LIPOPROTEINS IN RENAL-FAILURE AND DURING HEMODIALYSIS

Contact to artificial surfaces during hemodialysis activates leukocyte s, which then form oxidized arachidonic acid products and free radical s. This might promote the oxidative modification of low-density lipopr oteins (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 hemodialysi s. Therefore monitored LDL and high-density lipoprotein (HDL) resistan ce to copper-stimulated oxidation in patients with end-stage renal dis ease on maintenance hemodialysis with cellulose acetate or polysulfone membranes (n = 12), in patients with chronic renal failure (n = 13) a nd in healthy controls (n = 12). Six of the dialysis patients were res tudied during a single cuprophane dialysis. Circulating leukocytes wer e reversibly reduced early in hemodialysis with cellulose acetate (min imum, 83.6% +/- 7.4% of baseline values at 30 minutes after dialysis s tart), 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). De spite the leukocyte activation, LDL oxidation lag time was not shorten ed in comparison with healthy controls and was even prolonged at the e nd 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 6 0 minutes after start of hemodialysis and returned to predialysis valu es thereafter. In patients with chronic renal failure, the lag time of HDL oxidation was significantly prolonged (13.34 minutes +/- 0.9) com pared 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). The similar pattern among these groups in LDL oxidation just missed overall significance (P = 0.07). Therefore, neither LDL no r HDL antioxidative defenses are compromised by hemodialysis-associate d leukocyte activation. The prolonged lag phase of HDL oxidation early after the start of hemodialysis may be related to heparin-induced lip oprotein lipase activity with rapid lipid changes in HDL composition. The increased antioxidative defense of lipoproteins in chronic renal f ailure appears to be related to the retention of reducing metabolic en d products. (C) 1995 by the National Kidney Foundation, Inc.