ABSTRACT
Cell adherence to plate dialyzer membranes was analyzed at the end of 4 hours of dialysis. Three types of membranes were examined: Cuprophan Hemophan and Gambrane, (a polycarbonate membrane). The membranes were mounted in dialyzers that contained 23 layers of one membrane type and one layer of each of the two other. Less leukocytes adhered to the Pc than to the Cu and He membranes. Transient initial complement activation during dialysis, which was considerably lower with dialysers containing mainly Pc membrane, was not correlated to adherence of cells to the membranes. Instead flow geometry is proposed as the main factor determining the adherence. Contrary to what has been earlier suggested, we think that leukocyte adherence is not a very suitable measure of membrane biocompatibility. The reason is that the influence of membrane surface-chemical factors can not be separated from mechanical factors due to the design of the device.
Subject(s)
Biocompatible Materials , Leukocytes/physiology , Membranes, Artificial , Renal Dialysis/instrumentation , Cell Adhesion/physiology , Cellulose/analogs & derivatives , Humans , PolymersABSTRACT
A high blood flow of 400 ml/min induces leukocytosis after 2 hr of dialysis with leukocyte concentrations of 110-150% of predialysis values. The leukocytosis occurs with both low and high biocompatible membranes, such as Cuprophan, Hemophan, and Polyamide. Cuprophan induces the most profound leukopenia, and also induces the most pronounced leukocytosis. For treatments with a given membrane there was, however, no correlation between leukopenia and leukocytosis. Leukopenia was independent of blood flow, while leukocytosis was strongly influenced by this factor. These observations indicate that different factors cause leukopenia and leukocytosis. Although a larger area induced more leukopenia, the effect was small. Membrane area had no effect on leukocytosis. There were no acute clinical side effects during dialysis that could be related to the leukocyte overshoot. The cause and chronic clinical consequences of leukocyte overshoot are unknown.
