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Intraperitoneal fibrin-formation and its inhibition in CAPD

E Gries, D Paar, N Graben

    Clinical Nephrology
    |October 1, 1986
    PubMed

    Insights

    Intraperitoneal heparin effectively inhibits fibrin formation in continuous ambulatory peritoneal dialysis (CAPD) patients by activating antithrombin III. This study confirms heparin

    Area of Science:

    • Biochemistry
    • Nephrology
    • Hematology

    Background:

    • Fibrin formation is a concern in continuous ambulatory peritoneal dialysis (CAPD).
    • Heparin is used to inhibit fibrin formation during CAPD.
    • The mechanism of heparin's action in the peritoneal cavity requires further investigation.

    Purpose of the Study:

    • To investigate intraperitoneal fibrin formation and its inhibition by heparin in CAPD patients.
    • To determine the concentration and behavior of heparin and antithrombin III in the peritoneal dialysate.
    • To assess the role of antithrombin III in heparin-mediated fibrin inhibition.

    Main Methods:

    • Six CAPD patients were studied.
    • Intraperitoneal heparin (5000 U) was administered.
    • Concentrations of heparin, antithrombin III, and fibrinopeptide A were measured in plasma and dialysate over a 4-hour dwell time.
    • In vitro experiments assessed fibrin formation inhibition by heparin without antithrombin III.

    Main Results:

    • Intraperitoneal heparin concentration decreased over 4 hours.
    • Antithrombin III concentration in dialysate increased and was sufficient for its function.
    • Fibrinopeptide A levels were significantly elevated in dialysate during regular CAPD but decreased after heparin administration.
    • Heparin showed minimal fibrin inhibition in vitro without antithrombin III.

    Conclusions:

    • Fibrin formation, indicated by elevated fibrinopeptide A, occurs intraperitoneally in CAPD patients.
    • Antithrombin III present in the dialysate is sufficient to potentiate heparin's anticoagulant effect.
    • Intraperitoneal heparin effectively inhibits fibrin formation in CAPD by accelerating the action of antithrombin III.

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