Unbound MEDLINE

Hemostasis, platelet function and serotonin in acute and chronic renal failure. Thrombosis research. [Thromb Res] Journal article

 
TitleHemostasis, platelet function and serotonin in acute and chronic renal failure.
Author(s)Malyszko J, Malyszko JS, Pawlak D, Pawlak K, Buczko W, Mysliwiec M 
InstitutionDepartment of Nephrology, Bialystok Medical School, Poland.
SourceThromb Res 1996 Sep 1; 83(5):351-61.
MeSHAdenosine Diphosphate
Adolescent
Adult
Aged
Antiplasmin
Antithrombin III
Arachidonic Acid
Blood Platelets
Collagen
Comparative Study
Female
Fibrinolysis
Fibronectins
Hemostasis
Humans
Kidney Failure, Acute
Kidney Failure, Chronic
Lipoprotein(a)
Male
Middle Aged
Peptide Fragments
Peptide Hydrolases
Plasmin
Plasminogen Activator Inhibitor 1
Platelet Aggregation
Prothrombin
Renal Dialysis
Research Support, Non-U.S. Gov't
Ristocetin
Serotonin
Tissue Plasminogen Activator
von Willebrand Factor
AbstractA pathogenetic role for fibrin deposition and platelet activation in the kidney is thought to play a role in the pathogenesis of acute renal failure (ARF). Thus, some fibrinolytic parameters and platelet function have been studied in 17 patients with ARF and compared to healthy volunteers and subjects with chronic renal failure (CRF). Since serotonin may participate in pathological processes resulting from platelet/vessel wall interactions, its level in the whole blood and plasma was also assayed. In ARF and CRF platelet aggregatory responses in both whole blood and in platelet rich plasma upon stimulation with various agonists (collagen, arachidonic acid, ADP, ristocetin) were lower than those obtained in healthy volunteers. Increased levels of lipoprotein (a), von Willebrand factor (vWF) and fibronectin were found in ARF relative to controls. Protein C activity was significantly lower in patients with ARF. Euglobulin clot lysis time was prolonged in ARF and CRF, reflecting a decreased overall fibrinolytic activity. Activity of tissue plasminogen activator (tPA) inhibitor (PAI) and PAI:Ag were higher in ARF, whereas tPA:Ag, urokinase, tPA/PAI complexes, thrombin-antithrombin complexes (TAT), plasmin-antiplasmin (PAP) complexes, fibrinogen, and F1+2 did not differ between ARF and controls. In CRF elevated levels of TAT, PAP, fibrinogen and prothrombin fragments F1+2 were found, whereas concentration of fibronectin was lowered when compared to controls. In both groups of renal failure patients increased levels of fibrin monomers and d-dimer were found relative to healthy volunteers. Whole blood serotonin was significantly lower, whereas plasma serotonin was significantly higher in patients with ARF and CRF relative to controls. Serotonin uptake and its release from platelets were markedly diminished in patients with ARF and CRF. Chronic renal failure exhibit a slightly different pattern of coagulopathies that acute renal failure.
Languageeng
Pub Type(s)Journal Article
PubMed ID8873344
  
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