Hemostasis, platelet function and serotonin in acute and chronic renal failure.
A 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.
Malyszko
J
J
Department of Nephrology, Bialystok Medical School, Poland.
Malyszko
J S
JS
Pawlak
D
D
Pawlak
K
K
Buczko
W
W
Mysliwiec
M
M
D058186:Acute Kidney Injury / Q000097:blood*; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000990:Antithrombin III / Q000032:analysis; D016718:Arachidonic Acid / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D003094:Collagen / Q000494:pharmacology; D005260:Female; D005341:Fibrinolysin / Q000032:analysis; D005342:Fibrinolysis; D005353:Fibronectins / Q000032:analysis; D006487:Hemostasis; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy; D017270:Lipoprotein(a) / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D010974:Platelet Aggregation / Q000187:drug effects; D011516:Prothrombin / Q000032:analysis; D006435:Renal Dialysis; D012310:Ristocetin / Q000494:pharmacology; D012701:Serotonin / Q000097:blood*; D010959:Tissue Plasminogen Activator / Q000032:analysis; D000979:alpha-2-Antiplasmin / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
D005353:Fibronectins; D017270:Lipoprotein(a); D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C045879:prothrombin fragment 1.2; D014841:von Willebrand Factor; D012310:Ristocetin; D016718:Arachidonic Acid; D012701:Serotonin; D000244:Adenosine Diphosphate; D000990:Antithrombin III; D011516:Prothrombin; D003094:Collagen; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin