Key result
Hemodialysis is linked to ~24 percentage point lower albumin binding efficiency.
Why the study?
Malnutrition, physical inactivity, uremic toxins, and inflammation common in chronic kidney disease patients may decrease lipoprotein lipase activity, especially in those on hemodialysis, but the impact of hemodialysis and anticoagulation on LPL function and albumin binding properties is not fully understood.
Observational (n=58)
Yes
May compromise toxin handling post-hemodialysis; leaves open whether heparin alternatives preserve albumin function in trials.
Factors such as malnutrition, physical inactivity, uremic toxins, and inflammation are known to influence the activity of lipoprotein lipase (LPL), an important enzyme in metabolism of blood lipids. In patients with chronic kidney disease these factors are common and may result in a decreased LPL activity. This is particularly so in patients on hemodialysis. Further, during each dialysis treatment, the use of heparin (or low molecular weight heparin) induces a release of LPL from its normal binding sites at the plasma membrane of endothelial cells. This results in an increased degradation of the enzyme and a relative lack of LPL activity for up to 10 hours from the start of the dialysis. Thus, the use of conventional anticoagulation for hemodialysis, in addition to the consequences of the uremic state, may cause a severe functional deficiency of LPL. This in turn may have deleterious effects on energy metabolism and may contribute to the increased risk for cardiovascular disease in this vulnerable group of patients.
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Stegmayr et al. (2009) conducted an observational in Maintenance hemodialysis (n=58). Hemodialysis vs. Pre-hemodialysis baseline was evaluated on Albumin binding efficiency (BE) (95% CI -23.7 to -14.0, p=<0.001). Hemodialysis significantly decreased median albumin binding efficiency from 52% to 28% and median detoxification efficiency from 38% to 11% (p<0.001).
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