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The hemodialysis membrane surface serves as the semipermeable interface between blood and dialysate, facilitating the removal of toxins and excess fluid in patients with end-stage renal disease (ESRD) (Ronco et al., 2017, Nature Reviews Nephrology). Composed of materials such as polysulfone, polyethersulfone, or cellulose triacetate, these surfaces are engineered to mimic biological membranes but often trigger the contact phase of the coagulation cascade and the alternative complement pathway upon exposure to blood (Kourtzelis et al., 2010, Blood). This bioincompatibility can lead to systemic inflammation, oxidative stress, and thrombotic events, making the surface a primary target for pharmacological and engineering modifications (Bowry & Gatti, 2011, International Journal of Artificial Organs). Pharmacological strategies include the use of systemic anticoagulants like heparin or the development of bioactive membranes coated with Vitamin E or heparin to improve hemocompatibility (D'Ambrosio et al., 2017, Journal of Nephrology). Understanding the molecular interactions at this surface is crucial for reducing cardiovascular morbidity and improving long-term outcomes for dialysis patients (Morena et al., 2002, Kidney International).
Surface adsorption and inhibition of the coagulation cascade via systemic or surface-bound anticoagulants, and reduction of oxidative stress through antioxidant coatings.
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