Reduction of platelet glycoprotein Ib in uraemia

Sloand, EM; Ja, Sloand; Prodouz, K. N.; Hg, Klein; Mw, Yu; Harvath, Liana; Fricke, William

doi:10.1111/j.1365-2141.1991.tb08587.x

Cited by 62 publications

(31 citation statements)

References 29 publications

(7 reference statements)

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“…just as reported by Sloand ct al. [2], We agree with these data, that clarify the important role of a defect in primary hemo stasis in the pathogenesis of uremic bleeding. We investigated the abnormalities of platelet surface glycoproteins GPIb, the receptor for von Willebrand factor, and GPIIb/llla.…”

supporting

confidence: 76%

Platelet Glycoproteins GPIb and GPIIb/llla Abnormalities in Uremia

Liani¹,

Salvati

Golato³

et al. 1996

Nephron

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Dear Sir, In a recent article by Nomura et al.[1] a reduction of platelet glycoprotein GPIb ex pression in the uremic patient was con firmed. just as reported by Sloand ct al. [2], We agree with these data, that clarify the important role of a defect in primary hemo stasis in the pathogenesis of uremic bleeding. We investigated the abnormalities of platelet surface glycoproteins GPIb, the receptor for von Willebrand factor, and GPIIb/llla. the receptor for fibrinogen, since the early stages of renal failure and we correlated them with the degree of uremia and plasma creatinine. We studied four groups of patients: group A (n = 18 healthy controls) creatinine = 0.8 ± 0.3 mg%; group B (n = 10) creatinine = 1.8 ± 0.5 mg%; group C (n = 8) creatinine = 5.4 ± 2.1 mg%; group D (n = 10) creatinine = 9.6 ± 3. In all the patients we investigated platelet glycoproteins GPIb and GPIIb/llla with monoclonal antibodies CD42b and CD41 (Biorad, Italy) and flow cytometric analysis (Bryte cytometer: Biorad). Mean values of GPIb glycoproteins (mean flow ± SD): group A = 43.09 ± 11.19; group B = 37.84 ± 5.57: group C = 34.82 ± 9.54 (p < 0.05); group D = 33.02 ± 7.6 (p < 0.05). Mean values of GPIIb/llla: group A = 312.40 ± 108.3: group B = 410.63 ± 34.65 (p < 0.05); group C = 434.89 ± 50.86 (p < 0.025); group D = 415.31 ± 70.5 (p< 0.05). Our data suggest: (1) that platelet surface gly coprotein abnormalities are present since the early stages of renal failure and are well cor related with the degree of uremia; (2) that also glycoprotein GPIIb/llla is altered in uremia (these further data are different from the data reported by other authors), and (3) that the defect is not corrected by dialytic procedure. Finally, we want to stress in ure mic patients the main importance of platelet glycoprotein abnormalities that also have an important role in the abnormal procoagulant response to treatment with recombinant hu man erythropoietin, as just reported [3].

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supporting

confidence: 76%

Platelet Glycoproteins GPIb and GPIIb/llla Abnormalities in Uremia

Liani¹,

Salvati

Golato³

et al. 1996

Nephron

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“…On the other hand, the use of methods such as RiCoF activity and RIPA PRP in some studies suggests depressed vWF activity [17, 18, 19], not confirmed by other workers [10, 11, 15, 20]. The expression of GP Ib on platelets of HD patients was also described as being either normal [21, 22, 23] or diminished [15, 24, 25]. The low plasmatic vWF activity could be partially explained by the decrease in the hemostatically most effective high-molecular-weight multimers of vWF [20, 26], although this has not been confirmed by other investigators [15, 27].…”

Section: Discussionmentioning

confidence: 99%

Comparison of Different Assays for von Willebrand Factor in Hemodialysis Patients

Borawski

Pawlak²,

Myśliwiec³

2000

Pathophysiol Haemos Thromb

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Von Willebrand factor (vWF) abnormalities are involved in the hemostatic disturbances of uremia. Studies of vWF in both anemic and recombinant erythropoietin (EPO)-treated maintenance hemodialysis (HD) patients have given inconsistent results that could be partially dependent on the methodology. Therefore, the reciprocal relationships between four different vWF assays were studied in HD patients in relation to EPO therapy. Plasma vWF activity measured by ELISA using monoclonal antibodies against platelet glycoprotein (GP) Ibα (vWF:Act), plasma vWF antigen concentration by ELISA employing polyclonal antihuman vWF antibodies (vWF:Ag), and functional vWF activity by ristocetin-induced platelet aggregation (RIPA) in both platelet-rich plasma (PRP) and whole blood were studied in 70 HD patients. In the whole group, no correlations between these assays were found. In the non-EPO patients (n = 32), vWF:Act was correlated with vWF:Ag (r = 0.504, p = 0.003) but not with vWF activity by RIPA in PRP. In the EPO-treated patients (n = 38), vWF:Act was higher than in the untreated ones (p = 0.001), and vWF:Ag was related to the whole-blood RIPA (r = 0.386, p = 0.016). In conclusion, the platelet GP Ibα-binding epitope of the vWF molecule assessed by vWF:Act ELISA is intact in HD patients. However, this assay does not reflect the functional vWF activity as measured by RIPA in PRP. In EPO-treated patients, the GP Ibα-binding domains of vWF are more available but the plasmatic vWF monomers are neither more numerous by vWF:Ag ELISA nor more hemostatically active by RIPA PRP. The whole blood RIPA test has some potential for the quantification of vWF monomers in EPO-treated HD patients.

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“…We also found a significant decrease in mean platelet volume in uremic platelets (data not shown), but they only represented 7% of the mean platelet volume of normal platelets. Other platelet membrane components, like glycoprotein Ib measured by immunoblotting, have been reported to be decreased in uremia [7], while the decreased expression of glycoproteins IIb-IIIa seems to be the consequence of a functional defect [8, 9, 10]. The reasons for a diminution of the platelet components are unclear, but defects in membrane synthesis or platelet fragmentation have been proposed as the most plausible mechanisms [7].…”

Section: Discussionmentioning

confidence: 99%

“…Other platelet membrane components, like glycoprotein Ib measured by immunoblotting, have been reported to be decreased in uremia [7], while the decreased expression of glycoproteins IIb-IIIa seems to be the consequence of a functional defect [8, 9, 10]. The reasons for a diminution of the platelet components are unclear, but defects in membrane synthesis or platelet fragmentation have been proposed as the most plausible mechanisms [7]. The platelet content of cholesterol was similar to the values found in normal platelets, and therefore, the cholesterol:phospholipid ratio of these cells in uremia was high.…”

Section: Discussionmentioning

confidence: 99%

“…Decreased adhesion to subendothelium [1, 2], impaired formation of thromboxane [3, 4] and abnormal aggregation response to agonists [2, 3, 4, 5, 6] have been well documented. In addition, other structural defects, like a decrease in expression of membrane glycoproteins [7, 8, 9, 10] and dense granule content [4] have been described. Changes in plasma lipoproteins [11] and alterations in red cell membrane lipids [12] have also been documented in these patients.…”

Section: Introductionmentioning

confidence: 99%

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Lipid Composition of Platelets in Patients with Uremia

Vecino

Navarro-Antolı́n

Teruel

et al. 1998

Nephron

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Aims: The lipid composition of platelets and the function of these cells in patients with uremia were studied. Methods: Fourteen patients and 14 normal volunteers were studied. Platelet lipids including phospholipids and cholesterol, as well as the platelet aggregation response to agonists, were studied. Results: The amount of platelet phospholipids was decreased in patients compared to controls (338.0 ± 79 vs. 511.6 ± 125 nmol/10⁹ cells; p < 0.001), while the percentage of the five main specimens of these compounds was normal. The content of platelet cholesterol in patients (97.8 ± 17.0 µg/10⁹ cells) was similar to that in controls (91.7 ± 26.0 µg/10⁹ cells). Consequently, the cholesterol:phospholipid ratio in uremic platelets was increased (0.75 ± 0.1 vs. 0.46 ± 0.1; p < 0.01). Although this feature is associated with hyperreactive platelets, the aggregation tests were defective for adenosin diphosphate (p < 0.01), arachidonic acid (p < 0.01), epinephrine (p < 0.01) and collagen (p < 0.001). This behavior is probably due to the multifactorial platelet defect described in uremia.

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Reduction of platelet glycoprotein Ib in uraemia

Cited by 62 publications

References 29 publications

Platelet Glycoproteins GPIb and GPIIb/llla Abnormalities in Uremia

Platelet Glycoproteins GPIb and GPIIb/llla Abnormalities in Uremia

Comparison of Different Assays for von Willebrand Factor in Hemodialysis Patients

Lipid Composition of Platelets in Patients with Uremia

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