scholarly journals Abnormal platelet function in children with chronic renal failure undergoing hemodialysis.

1991 ◽  
Vol 4 (1) ◽  
pp. 67-75
Author(s):  
Yoshio Ishikawa ◽  
Hiroshi Kawaguchi ◽  
Katsuimi Itoh
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Platelet Function

Tranexamic Acid Inhibits Fibrinolysis, Shortens the Bleeding Time and Improves Platelet Function in Patients with Chronic Renal Failure

1999 ◽  
Vol 82 (10) ◽  
pp. 1250-1254 ◽  
Author(s):  
Olga Panes ◽  
Blanca Muñoz ◽  
Edgar Pais ◽  
Rodrigo Tagle ◽  
Fernando González ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Platelet Aggregation ◽  
Tranexamic Acid ◽  
Platelet Function ◽  
Bleeding Time ◽  
Degradation Products ◽  
Severe Disease ◽  
Plasmin Activity ◽  
Primary Hemostasis

Summary Background: A defect in platelet function is the main determinant of the prolonged bleeding time in chronic renal failure (CRF). We previously reported a significant correlation between platelet abnormalities and elevated plasma markers of plasmin and thrombin generation. Our aim was to explore the effect of inhibiting both plasmin action with tranexamic acid (TA) and thrombin production with low molecular weight heparin (LMWH), on the bleeding time (BT) and platelet function in patients with CRF. Methods: 37 patients with CRF (mean creatinine 8.6 ± 4.4 mg/dl) under conservative treatment, with prolonged BT, entered this study and received TA during 6 days, with (n = 24) and without LMWH (n = 13). BT, platelet aggregation/secretion, platelet granule contents, von Willebrand factor and parameters of coagulation and fibrinolysis were recorded before and at the end of treatment. Results: The BT was shortened in 26/37 (67%) patients. This effect was associated with significant improvement of platelet aggregation and secretion, with decrease to a normal range of fibrin/fibrinogen degradation products, mild increase in plasmin-antiplasmin complexes and pronounced reduction of circulating plasminogen. No differences were seen among patients with or without LMWH. No serious side effects or complications were observed. Interpretation: These findings indicate that the activation of fibrinolysis plays a significant role in the defect of primary hemostasis in patients with CRF. Inhibition of plasmin activity with TA shortens the BT and improves platelet function in the majority of patients with severe disease.

scholarly journals Impaired function of platelet membrane glycoprotein IIb-IIIa in end-stage renal disease.

1994 ◽  
Vol 5 (1) ◽  
pp. 36-46
Author(s):  
M P Gawaz ◽  
G Dobos ◽  
M Späth ◽  
P Schollmeyer ◽  
H J Gurland ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Uremic Toxin ◽  
Bleeding Tendency ◽  
Fibrinogen Receptor ◽  
Fibrinogen Binding ◽  
Uremic Patients ◽  
Stage Renal Disease

Impaired platelet function and a bleeding tendency are well-recognized complications of chronic renal failure. Because the fibrinogen receptor GPIIb-IIIa plays a central role in platelet aggregation and adhesion to the subendothelium, it was reasoned that a defect in this receptor may underlie the impaired platelet function in uremia. To test this hypothesis, the function of this receptor in the platelets of 11 uremic patients was studied. Aggregation studies were performed with flow cytometric techniques with anti-GPIIb-IIIa conformation-specific monoclonal antibodies (mAb) (anti-LIBS1 and anti-PMI-1). Antifibrinogen and antithrombospondin mAb were used to characterize fibrinogen binding to GPIIb-IIIa and the release of alpha-granules, respectively. Platelets from patients with chronic renal failure showed significantly decreased binding of conformation-dependent anti-LIBS1 mAb after ADP, phorbol myristate acetate, or RGD-peptide stimulation compared with normal controls, suggesting a defect related to the ability of the fibrinogen receptor to undergo a conformational change. Moreover, antifibrinogen and antithrombospondin binding to activated platelets were reduced in uremic patients, implying impairment of both ligand-binding and alpha-granule release. Hemodialysis partially restored GPIIb-IIIa function, which may account for the observed effects of this therapy in restoring platelet aggregation. These findings indicate that platelets of patients with chronic renal failure reveal an aggregation defect at least partially due to an intrinsic GPIIb-IIIa dysfunction and the presence of a putative uremic toxin that inhibits fibrinogen binding to GPIIb-IIIa.

HEMOSTASIS, PLATELET FUNCTION AND SEROTONIN IN ACUTE AND CHRONIC RENAL FAILURE

1996 ◽  
Vol 83 (5) ◽  
pp. 351-361 ◽  
Author(s):  
J. Malyszko ◽  
J.S. Malyszko ◽  
D. Pawlak ◽  
K. Pawlak ◽  
W. Buczko ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Platelet Function
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