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The nephrotic syndrome in humans is associated with an increased risk for arterial and venous thrombosis, the pathogenesis of which appears to be very complex. We have developed an experimental model of nephrotic syndrome in rats which follows a single i.v. injection of adriamycin (AIM, 5-10 mg/kg b.w.). Starting from 2 weeks after ADM-injection, rats showed a remarkably increased susceptibility to thrombotic stimuli; indeed, the occlusion time of a polyethylene cannula inserted in the abdominal aorta was 22±15 hours in treated animals versus 62±5 in control animals (n=16, p&lt; 0.001). Concomitantly the rats showed: increased plasma fibrinogen and factor VIII: C activity, shortened APTT, low antithrombin and markedly depressed fibrinolytic activity. Moreover, platelet-rich plasma (PRP) of treated rats produced significantly higher amounts of both malondialdehyde (MDA) (spectrophotometric assay) and thromboxane B2 (RIA) in response to AA. When MDA generation was studied with a kinetic approach, the PRP of nephrotic animals had significantly lower apparent Km for AA in respect to the controls (0.15 ± 0.07 mM AA versus 0.90 ± 0.25 mM AA, p&lt;0.01). Washed platelets from both groups, in contrast, showed similar Km values for AA (0.10 mM ± 0.04 versus 0.12 ± 0.03).  MDA generation by washed normal platelets resuspended in plasma was normal if plasma had been collected 1 or 3 days after ADM administration but was already significantly higher with plasma collected 5, 7 or 14 days after treatment. The concomitant mild hypoalbuminemia does not completely account for this plasma abnormality. Thus, in the model, an abnormal plasmatic modulation of platelet AA metabolism could be detected much earlier than the coagulation/fibrinolysis changes and the hypersensitivity to thrombotic stimuli.

thrombosis and haemostasis

Disturbed Plasmatic Modulation Of Arachidonic Acid (AA) Metabolism In Platelets From Rats With Nephrotic Syndrome: An Early Parameter Of Thrombotic Risk?