1990
DOI: 10.1016/0009-8981(90)90280-6
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A compensatory mechanism improving red cell membrane fluidity in hemodialysed patients

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Cited by 8 publications
(6 citation statements)
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“…Decreases in total and LDL-cholesterol have been shown to be associated with a relative increase in SFA and decrease in PUFA in patients with renal failure on haemodialysis, and after plasmapheresis in subjects with familial hypercholesterolaemia (Brook et al 1983, Peuchant et al 1990). Although this mechanism remains a possibility, no correlation between the changes in platelet membrane fatty acids and those in serum lipoproteins was observed in this study.…”
Section: Discussionmentioning
confidence: 98%
“…Decreases in total and LDL-cholesterol have been shown to be associated with a relative increase in SFA and decrease in PUFA in patients with renal failure on haemodialysis, and after plasmapheresis in subjects with familial hypercholesterolaemia (Brook et al 1983, Peuchant et al 1990). Although this mechanism remains a possibility, no correlation between the changes in platelet membrane fatty acids and those in serum lipoproteins was observed in this study.…”
Section: Discussionmentioning
confidence: 98%
“…Decreased enzyme activity has been suggested to be the consequence of the presence of various endogenous digoxin-like factors ( E D L F ) (6)(7)(8). Altered physicochemical properties of human erythrocyte membranes in uraemic patients (9,10) could also result in changes in enzyme activity. In spite of these data the mechanism of decreased N;i+-K+ ATPase activity in uraemia remains to be clarified.…”
mentioning
confidence: 99%
“…Since EDLF may be involved in the regulation of Na + /K + ATPase activity, one may speculate that endogenous Na + pump inhibitors could be the reason for the decreased enzyme activity in uremic children and adolescents. However, the lack of direct correlation between EDLF and Na + pump inhibition suggests that the regulation of the Na + /K + ATP-ase activity is more complex, including other possible inhibitors and/or the alteration of lipid microenvironment of the enzyme [7,11]. Similarly, the lack of correlation between blood pressure and EDLF suggests that EDLF does not play a central role in the hypertension of CRF.…”
Section: Discussionmentioning
confidence: 79%
“…Its impairment results in significant changes in intra-and extracellular volume and cationic homeostasis. In cases of lower Na + /K + ATP-ase activity the intracellular Ca 2+ elevates, leading to higher blood pressure and enhancement of myocardial contractility [8,9,10,11].…”
Section: Introductionmentioning
confidence: 99%