Effects of L-carnitine on sodium transport in erythrocytes from dialyzed uremic patients

Abstract

Red blood cell (RBC) sodium transport systems were studied by cation flux methodology, measuring both the ouabain-sensitive Na-K pump and the ouabain-insensitive Na-K cotransport (CoT), as well as the Na-lithium (Li) countertransport (CTT), in eight patients on chronic hemodialysis and a control group of eight normal individuals. Intracellular sodium content and passive Na permeability were also determined. The effect of L-carnitine on RBC sodium transport in the uremic group was evaluated by supplementation with oral (1 g/day) and i.v. (1 g post-hemodialysis) L-carnitine for 60 days. Mean Na efflux through the ouabain-sensitive Na-K pump was 30.7% lower in uremic patients than in controls (3.49 ± 1.52 vs. 5.04 ± 0.72 mmol/liter RBC x hr; P < 0.025). Intracellular Na content was higher in uremic patients (11.57 ± 3.38 vs. 8.86 ± 0.88 mEq/liter RBC; P < 0.05), but no differences were found in Na-K CoT, Na-Li CTT or passive Na permeability. L-carnitine treatment increased the ouabain-sensitive Na efflux in uremic patients (4.76 ± 1.6 vs. 3.49 ± 1.52 mmol/liter RBC x hr; P < 0.05), with no change in CoT, CTT, intracellular Na content or passive Na permeability. We conclude that L-carnitine deficiency may play a major role in uremic Na-K pump disfunction.