Increase of erythrocyte resistance to hemolysis and modification of membrane lipids induced by hemodialysis

Peuchant, Evelyne; Salles, Christine; Vallot, C; Wone, C; Jensen, Raymond

doi:10.1016/0009-8981(88)90235-5

Cited by 25 publications

(19 citation statements)

References 40 publications

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“…The reason why the osmotic fragility improved after dialysis may be attributed to the normalization of biochemical parameters such as urea nitrogen, creatinine, other cations, and serum osmolarity. Our results were in good agreement with those reported previously [12, 13, 14]. …”

Section: Discussionsupporting

confidence: 83%

Red Blood Cell Osmotic Fragility in Chronically Hemodialyzed Patients

Wu¹,

Jeng²,

Wei³

et al. 1997

Nephron

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Chronic renal failure induces anemia and a short erythrocyte life span. Red blood cell (RBC) osmotic fragility is the resistance of RBC hemolysis to osmotic changes that is used to evaluate RBC friability. To find the cause of shortened red cell survival in uremic patients, we evaluated the RBC osmotic fragility in 57 chronic hemodialyzed patients. Each patient had received 12 h of dialysis per week continuously prior to being enrolled in the study. Nineteen healthy volunteers served as a control group. Biochemistry, hemoglobin, electrolyte, osmolarity, β₂-microglobulin, and intact parathyroid hormone were examined before and after the dialysis session. To evaluate the osmotic fragility of RBC, blood samples were collected in heparinized test tubes. Fifty microliters of the RBC of each individual was then incubated in solutions containing a series of various concentrations of NaCl ranging from 0 to 0.6%. The concentration of NaCl at which 50% of RBCs were lysed was considered the median osmotic fragility (MOF). The results showed that the MOF was significantly greater in hemodialyzed patients before dialysis than in the control group (0.41 ± 0.03 vs. 0.39 ± 0.02%). The osmotic resistance to hemolysis was also recorded after dialysis (MOF 0.38 ± 0.03%). Correlation analysis showed that the MOF was significantly correlated with urea nitrogen, serum osmolarity, and intact parathyroid hormone level. In addition, the osmotic fragility was higher in patients who had a predialysis intact parathyroid hormone level >100 pg/dl. In conclusion, hemodialysis can improve the osmotic fragility. The mechanism underlying this improvement may be the removal of low molecular weight uremic toxins, resulting in normalization of serum osmolarity. Our results indicate that parathyroid hormone is probably a major factor influencing RBC osmotic fragility in chronic renal failure.

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Section: Discussionsupporting

confidence: 83%

Red Blood Cell Osmotic Fragility in Chronically Hemodialyzed Patients

Wu¹,

Jeng²,

Wei³

et al. 1997

Nephron

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“…The hemolytic activity of saponins, which are mixtures of plant glycosides, depends on the structure of glycoside molecules in commercial products [29]. The concentration of saponin, which hemolyzed 50% of red blood cells estimated to be 9.3 ± 0.6 mg/L [30]. The half maximal concentration that we found with the Merck product was in the same range (11.0 ± 1 mg/L).…”

Section: Hemolytic Reaction Caused By Tthrls or Saponin To Rabbit Erysupporting

confidence: 51%

“…The half maximal concentration that we found with the Merck product was in the same range (11.0 ± 1 mg/L). Either the use of red blood cells obtained from buffy coats or the incubation at 0 °C in our experiments instead of 37 °C [30] may explain the slightly higher resistance. …”

Section: Hemolytic Reaction Caused By Tthrls or Saponin To Rabbit Erymentioning

confidence: 93%

Development of an Antibody for Detection of Rhamnolipids Characterized as a Major Bacterial Virulence Factor

2013

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Rhamnolipids (RLs), the glycolipidic biosurfactants found initially as exoproducts of the opportunistic pathogen Pseudomonas aeruginosa, are characterized as virulence factors contributing to its pathogenesis infections. However, RLs are also produced by various bacterial species. They consist of a gluconic part, usually containing one or two rhamnoses, and a lipid part, containing one or two hydroxy-fatty acids. In this study, we present both the isolation of RLs from bacterial cultures of the non-pathogenic bacterium Thermus thermophilus as well as the development of the rabbit antibody directed against them. The antibody was titrated and evaluated, in respect of its recognition selectivity. Between both RLs constituents, it specifically recognized only the hydroxydecanoic acid between the fatty acids tested, contrary to rhamnose. The potential of the antibody to recognize both purified RLs and RLs present in crude extracellular media produced by T. thermophilus and Escherichia coli cultures, is evidenced by Dot Blot immuno-reaction. The development of this antibody is addressed in detail, as the sensitive analytical technique, and its potential use would facilitate the implementation of rhamnolipids' detection, or may be a useful and promising tool for determining these microbial secondary metabolites and virulence factors secreted in extracellular culture media or in biological fluids during infections.

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“…[8][9][10][11] Furthermore, a number of studies have reported that both the lipid and protein compositional profile of the RBC membrane is drastically modified during dialysis. [12][13][14][15] It is plausible to assume that these compositional modifications of the RBC membrane that are motivated by the extrinsic mechanisms [12][13][14][15] could somehow influence the membrane structure and ultimately influence the RBC lifespan. 5,6 Here we observed a negligible relative variation, -4% and +12% of the orifice and crevice indices, respectively, between the pre-and post-HD samples.…”

Section: Discussionmentioning

confidence: 99%

“…The possible mechanisms motivating and/or promoting the decreased lifespan of RBCs can be categorized as extrinsic (extracorporeal circuit) or intrinsic (uremic milieu). The extrinsic mechanisms relate to the extracorporeal circulation of the HD patient's blood during dialysis, since this can induce mechanical stress, 8,9 biochemical activation, 10,11 and membrane compositional modifications [12][13][14][15] to the RBCs. Intrinsic mechanisms refer to the interference of the biochemically crowded landscape of the RBC membranes (receptors, transport channels, etc) with the complex environment of uremic toxins.…”

Section: Stamopoulos Et Almentioning

confidence: 99%