The Permeability of Dialytic Membranes to Endotoxins: Clinical and Experimental Findings

Abstract

This study of 20 endotoxemic patients submitted to 70 hemodialyses (HD) found a reduction of the pre-HD limulus amebocyte lysate (LAL) positivity in 50 HD (71%), without appreciable differences in terms of effectiveness between cuprophan and AN 69 membranes. To define the mechanisms responsible for the reduction in LAL positivity during HD, the membranes were used in two in vitro studies, the first of which showed that the LAL positivity of blood containing lipopolysaccharide (LPS), submitted to hemofiltration (HF) for 300 min, remained unchanged and the ultrafiltrate remained constantly LAL negative. These results suggest that the reduction in LAL positivity observed in HD in vivo, an expression of reduced endotoxemia, cannot be attributed either to the filtration of the LPS as such or to its fragmentation following blood-membrane interaction into theoretically less filtrable molecules or to mechanisms of LPS adsorption on the membrane. The in vivo reduction of LAL positivity is more likely due to removal of the filtrable endotoxin fragments already released in the body, like lipid A, the biologically active component of LPS, known to react to LAL. This hypothesis was borne out by the second in vitro study, where the LAL positivity of blood containing lipid A, treated by HF for 80 min, gradually decreased, and dialytic permeability to lipid A was confirmed by the appearance of LAL positivity in the ultrafiltrate.

Water Treatment for Hemodialysis

“…Instead, it is more probable that endotoxins in dialysis fluid gain access to the patients' blood stream across the dialysis membrane [57,58],…”

Προγνωστικη Αξια Των Παραγοντων Κινδυνου Σε Ασθενεις Με Αποφρακτικο Ικτερο

“…Θεωρείται λοιπόν ότι απομάκρυνση από την κυκλοφορία του λιπιδίου Α με αιμοδιάλυση βοηθά στην πρόγνωση αυτών των ασθενών. 118 • 119 Η επίδραση των ενδοτοξινών στους νεφρούς προκαλεί αύξηση των νε φρικών αγγειακών αντιστάσεων, λόγω αγγειοσύσπασης, σε συνδιασμό με οίδημα του ενδοθηλίου των αγγείων, που με τη σειρά του προκαλεί βλάβη του ενδοθηλίου με αποτέλεσμα να χάνεται η αντιθρομβωτική ιδιότητα του και να προκαλούνται θρομβώσεις. 120 Ακόμη φαίνεται ότι απελευθερώνο νται κατεχολαμίνες που ενεργοποιούν το σύστημα ρενίνης -αγγειοτενσίνης καθώς επίσης και μικρού βαθμού διάχυτη ενδαγγειακή πήξη.…”