Hemostasis, platelet function and serotonin in acute and chronic renal failure

Area of Science:

• Nephrology
• Hematology
• Pathophysiology

Background:

• Fibrin deposition and platelet activation are implicated in acute renal failure (ARF) pathogenesis.
• Serotonin's role in platelet/vessel wall interactions warrants investigation in renal failure.

Purpose of the Study:

• To compare fibrinolytic parameters and platelet function in patients with ARF, chronic renal failure (CRF), and healthy controls.
• To assess whole blood and plasma serotonin levels and platelet serotonin handling in renal failure.

Main Methods:

• Studied 17 ARF patients, CRF patients, and healthy volunteers.
• Assayed platelet aggregatory responses to various agonists.
• Measured levels of lipoprotein (a), von Willebrand factor (vWF), fibronectin, Protein C, fibrinolytic markers, coagulation complexes, fibrin monomers, d-dimer, and serotonin.

Main Results:

• Reduced platelet aggregation in ARF and CRF compared to controls.
• Elevated lipoprotein (a), vWF, fibronectin, fibrin monomers, and d-dimer in ARF.
• Lower Protein C activity in ARF.
• Prolonged euglobulin clot lysis time, indicating decreased fibrinolysis in ARF and CRF.
• Increased tissue plasminogen activator inhibitor (PAI) in ARF.
• Elevated thrombin-antithrombin (TAT) and plasmin-antiplasmin (PAP) complexes in CRF.
• Altered whole blood and plasma serotonin levels in ARF and CRF.
• Diminished serotonin uptake and release by platelets in ARF and CRF.

Conclusions:

• ARF and CRF exhibit distinct coagulopathic patterns.
• Impaired platelet function and altered coagulation/fibrinolysis contribute to renal failure pathophysiology.
• Serotonin dysregulation and impaired platelet serotonin handling are observed in renal failure.