These findings align with known pathophysiologic mechanisms wherein elevated fibrinogen and acute phase reactants prolong APTT independent of heparin effect, hypertriglyceridemia causes spurious APTT prolongation through sample turbidity, renal dysfunction affects heparin clearance, and AT-III variability directly impacts heparin anticoagulant activity (33, 44–47). Here, SERPINC1 is linked to Abnormal renal physiology.