Aspects of Biocompatibility of Two Different Dialysis Membranes: Cuprophane and Polysulfone

Abstract

Intradialytic hypoxemia, leukopenia and coagulation system activation were monitored in 9 uremic patients during hemodialysis with cuprophane (Cu) and polysulfone (Psf) membranes, using the following parameters: polymorphonuclear count (PMN), elastase alpha-1 proteinase inhibitor (EI-alpha 1PI) complex, platelet count, beta-thromboglobulin (BTG), fibronectin (FN) and arterial oxygen tension (PaO2). Our results indicate that 1) intradialytic hypoxemia observed with both membranes does not seem to be exclusively related to the well-known membrane-dependent leukopenia; 2) platelet activation, as demonstrated by the plasma BTG increase, appears to be an exclusive cellulosic membrane-related phenomenon; 3) at the same time platelet activation seems to be the major factor responsible for high FN levels, the highest FN levels occurring concurrently with the lowest platelet count.

Platelet GPIIb/IIIa Is Activated and Platelet-Leukocyte Coaggregates Formed in vivo during Hemodialysis

“…These findings would mean that the stimuli causing the degranulation of platelets persist longer than the stimuli causing the conformational activation of GPIIb/IIIa during hemodialysis. Platelet activation during hemodialysis may be due to many factors, including shear stress, contact activation and agonist activation [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11]. Further examination is still needed to elucidate the more precise mechanism of platelet activation during hemodialysis.…”

“…During hemodialysis, the contact of blood with the prosthetic devices and the interaction of blood and artificial membranes result in platelet activation and a decrease in platelet cell count [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11]. The degree of platelet activation depends on the flow design of the dialysis membrane used [1, 2], the composition and geometry of the dialysis membrane [3, 4, 5, 6, 7, 8, 9, 10], and on rheological factors derived from blood circulation [11].…”

“…The degree of platelet activation depends on the flow design of the dialysis membrane used [1, 2], the composition and geometry of the dialysis membrane [3, 4, 5, 6, 7, 8, 9, 10], and on rheological factors derived from blood circulation [11]. In association with platelet activation, GPIIb/IIIa (CD41/CD61) is converted from a resting form into an activated form, in which its ligand-binding sites are exposed [12, 13, 14].…”

“…While some studies have reported the advantage of some synthetic membranes over cellulosic membranes in terms of platelet activation and platelet-leukocyte coaggregate formation [3, 4, 5, 6, 7, 26, 28], others have shown no differences in this regard [8, 9, 10]. Moreover, the tests used to study platelet function in clinical settings have their own limitations [15].…”

Biocompatibility and small protein permeability of hydrophilic-coated membrane dialyzer (NV) in hemodialysis patients: a pilot study

“…Although acute leukopenia is known to occur in all patients during the first 30 min of HD treatment [10], our study showed no reduction in the WBC during dialysis with either dialyzer. The platelet count usually decreases 5 to 15% at 15 to 30 min from the start of HD and recovers to the normal level by the end of the dialysis session [9,11]. Oshihara [3] reported that the numbers of platelets adhering to the membrane surface were lower with NV than with the conventional PS (CX) membrane.…”