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- W2044293011 abstract "Increased susceptibility to erythrocyte C5b-9 deposition and complement-mediated lysis in chronic renal failure.BackgroundDecreased red blood cell survival contributes to the anemia of chronic renal failure patients. Because patients on chronic dialysis therapy are frequently exposed to excessive complement activation, we investigated the susceptibility of this patient population to erythrocyte C5b-9 deposition, complement-mediated lysis, and ghost formation.MethodsWe developed a flow cytometric assay using antibodies to both glycophorin and the C5b-9 complex to detect C5b-9 deposition on intact erythrocytes and erythrocyte ghosts. Serum C5b-9 levels and C5b-9 deposition on erythrocyte ghosts were measured by enzyme-linked immunosorbent assay.ResultsA significant increase in C5b-9 deposition on intact erythrocytes was demonstrated in patients with advanced chronic renal failure (2.2±0.5%) and in patients on chronic maintenance hemodialysis (2.3±0.4%) compared with normal volunteers (0.9±0.1%, P = 0.005 vs. chronic renal failure, P < 0.001 vs. chronic hemodialysis patients). There was also a significantly higher percentage of C5b-9–positive erythrocyte ghosts in patients with advanced chronic renal failure (20.6±5%) and in chronic hemodialysis patients (15.5±3.1%) compared with normal controls (2.6±0.9%, P ≤ 0.001 vs. advanced chronic renal failure and chronic hemodialysis patients). Treatment of erythrocyte preparations with cobra venom factor, which activates the complement cascade, resulted in dramatic increases in the percentages of C5b-9–positive erythrocyte ghosts in patients with chronic renal failure (49.9±6.9%) and in chronic hemodialysis patients (45.0±4.2%) compared with normal volunteers (22.3±2.7%, P < 0.001 vs. chronic renal failure and chronic hemodialysis patients). Erythrocyte membrane expression of the complement regulatory proteins CD59 and CD55 did not significantly differ between normal controls and hemodialysis patients. Plasma C5b-9 levels after cobra venom factor stimulation were higher in chronic renal failure patients (538 μg/ml) compared with normal controls (345 μg/ml, P < 0.001).ConclusionsPatients with chronic renal failure and on hemodialysis therapy are susceptible to erythrocyte C5b-9 deposition with subsequent lysis and ghost formation. Susceptibility to complement-mediated erythrocyte injury may contribute to the anemia of chronic renal disease. Increased susceptibility to erythrocyte C5b-9 deposition and complement-mediated lysis in chronic renal failure. Decreased red blood cell survival contributes to the anemia of chronic renal failure patients. Because patients on chronic dialysis therapy are frequently exposed to excessive complement activation, we investigated the susceptibility of this patient population to erythrocyte C5b-9 deposition, complement-mediated lysis, and ghost formation. We developed a flow cytometric assay using antibodies to both glycophorin and the C5b-9 complex to detect C5b-9 deposition on intact erythrocytes and erythrocyte ghosts. Serum C5b-9 levels and C5b-9 deposition on erythrocyte ghosts were measured by enzyme-linked immunosorbent assay. A significant increase in C5b-9 deposition on intact erythrocytes was demonstrated in patients with advanced chronic renal failure (2.2±0.5%) and in patients on chronic maintenance hemodialysis (2.3±0.4%) compared with normal volunteers (0.9±0.1%, P = 0.005 vs. chronic renal failure, P < 0.001 vs. chronic hemodialysis patients). There was also a significantly higher percentage of C5b-9–positive erythrocyte ghosts in patients with advanced chronic renal failure (20.6±5%) and in chronic hemodialysis patients (15.5±3.1%) compared with normal controls (2.6±0.9%, P ≤ 0.001 vs. advanced chronic renal failure and chronic hemodialysis patients). Treatment of erythrocyte preparations with cobra venom factor, which activates the complement cascade, resulted in dramatic increases in the percentages of C5b-9–positive erythrocyte ghosts in patients with chronic renal failure (49.9±6.9%) and in chronic hemodialysis patients (45.0±4.2%) compared with normal volunteers (22.3±2.7%, P < 0.001 vs. chronic renal failure and chronic hemodialysis patients). Erythrocyte membrane expression of the complement regulatory proteins CD59 and CD55 did not significantly differ between normal controls and hemodialysis patients. Plasma C5b-9 levels after cobra venom factor stimulation were higher in chronic renal failure patients (538 μg/ml) compared with normal controls (345 μg/ml, P < 0.001). Patients with chronic renal failure and on hemodialysis therapy are susceptible to erythrocyte C5b-9 deposition with subsequent lysis and ghost formation. Susceptibility to complement-mediated erythrocyte injury may contribute to the anemia of chronic renal disease." @default.
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- W2044293011 date "1999-02-01" @default.
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- W2044293011 title "Increased susceptibility to erythrocyte C5b-9 deposition and complement-mediated lysis in chronic renal failure" @default.
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- W2044293011 cites W1598814826 @default.
- W2044293011 cites W1599283957 @default.
- W2044293011 cites W1967441433 @default.
- W2044293011 cites W1983084204 @default.
- W2044293011 cites W1984084256 @default.
- W2044293011 cites W1986604740 @default.
- W2044293011 cites W2001664656 @default.
- W2044293011 cites W2003989642 @default.
- W2044293011 cites W2008210540 @default.
- W2044293011 cites W2013345905 @default.
- W2044293011 cites W2027710810 @default.
- W2044293011 cites W2039353851 @default.
- W2044293011 cites W2049562611 @default.
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- W2044293011 cites W2056409867 @default.
- W2044293011 cites W2070047175 @default.
- W2044293011 cites W2071468645 @default.
- W2044293011 cites W2072998364 @default.
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- W2044293011 cites W2113313914 @default.
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- W2044293011 cites W2313842977 @default.
- W2044293011 cites W2334279733 @default.
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- W2044293011 cites W2417408226 @default.
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- W2044293011 doi "https://doi.org/10.1046/j.1523-1755.1999.00277.x" @default.
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