Clinical consequences of hemodialysis membrane biocompatibility
- Jeffrey S Berns, MD
Jeffrey S Berns, MD
- Editor-in-Chief — Nephrology
- Section Editor — Dialysis
- Professor of Medicine
- Perelman School of Medicine at the University of Pennsylvania
Interaction of the dialysis membrane with the components of blood has the potential to induce an inflammatory response and to lead to numerous long-term clinical sequelae that are in part determined by the degree of membrane biocompatibility. A biocompatible membrane (BCM) has traditionally been defined as "one that elicits the least amount of inflammatory response in patients exposed to it" . (See "Biochemical mechanisms involved in blood-hemodialysis membrane interactions".)
However, there is no standard technique for the measurement of biocompatibility. As a result, there are wide-ranging claims for biocompatibility by manufacturers of dialysis membranes based upon the testing method utilized, such as the generation of leukotrienes or the degree of complement activation.
Issues related to the clinical consequences of hemodialysis membrane biocompatibility are discussed in this topic review. Acute reactions to the hemodialysis membrane, such as that induced by ethylene oxide and complement activation are discussed separately. (See "Reactions to the hemodialysis membrane".)
TYPES OF HEMODIALYSIS MEMBRANES
There are three types of membranes currently used to manufacture dialyzers: cellulose, substituted cellulose, and synthetic noncellulose.
Cellulose — Cellulose, primarily manufactured as cuprophan (or cuprophane), is a polysaccharide-based membrane obtained from pressed cotton. It is composed of chains of glucosan rings with abundant free hydroxyl groups. Cupammonium is primarily used in the manufacturing process of this membrane (hence the name), but other methods of manufacturing exist.
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- TYPES OF HEMODIALYSIS MEMBRANES
- Substituted cellulose
- Synthetic noncellulose
- Determinants of biocompatibility
- ACUTE RENAL FAILURE
- CHRONIC RENAL FAILURE
- BETA-2 MICROGLOBULIN AND DIALYSIS-RELATED AMYLOIDOSIS
- PROTEIN CATABOLISM
- GENERAL INFLAMMATION
- LOSS OF RESIDUAL RENAL FUNCTION
- PULMONARY CHANGES