Biocompatibility study based on differential sequestration kinetics of CD14+CD16+blood monocyte subsets with different dialyzers

被引:9
作者
Griveas, Ioannis
Visvardis, George
Sakellariou, George
Passadakis, Ploumis
Thodis, Ilias
Vargemezis, Vasilios
Pavlitou, Aikaterini
Fleva, Aleka
机构
[1] Papageorgiou Gen Hosp, Dept Nephrol, Thessaloniki, Greece
[2] Univ Thrace, Sch Med, Dept Nephrol, Alexandroupolis, Greece
[3] Papageorgiou Gen Hosp, Dept Immunol, Thessaloniki, Greece
关键词
biocompatibility; CD14+CD16+monocytes; hemodialysis; dialyzers;
D O I
10.1080/08860220600781336
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The immune defect in hemodialysis (HD) patients is associated with a monocyte dysfunction, including an increase in the production of proinflammatory cytokines. Blood membrane contact leads to an increase in cellular activation and sequestration into the capillary bed of the lung. The influence of the sequestration on the number of mature monocytes was studied by analyzing the fate of monocytes, particularly, the CD14+CD16+ subpopulation, during HD treatment. In thirty stable HD patients, the distinct cell populations were determined by differential blood counts and flow cytometry. Patients with diabetes or systemic vasculitis, those showing evidence of infectious complications or malignancy, or those taking immunosuppressive medications were excluded from the study. Cells from this study population were analyzed before the start, 30 min thereafter, and at the end of HD treatment, each time using a different dialyzer: hemophan, methylmethacrylate ( PMMA), triacetate membrane, cuprophane/vitamin E, acrylonitrile, and sodium methallylsulfonate polymer (AN69). The CD14+CD16+ subset decreased at 30 min and remained suppressed for the course of dialysis. To examine whether currently used biocompatible membranes differ in their effect on the sequestration of monocyte subpopulations, temporal monocytic changes were comparatively analyzed during HD with a different dialyzer. The drop in the first 30 min until the end of HD treatment was significant (p < 0.05), very uniform, and sharp in all patients, and was independent upon membrane type. The CD14+CD16+ monocyte subpopulation showed increased and longer margination from the blood circulation during HD. Given the fact that CD14+CD16+ monocytes represent a sensitive marker for inflammation or cellular activation, the depletion of these cells may offer an easily accessible parameter that is more sensitive than complement activation for biocompatibility studies on forthcoming, improved dialyzer membranes.
引用
收藏
页码:493 / 499
页数:7
相关论文
共 28 条
[11]  
KAPLOW LS, 1968, J AMER MED ASSOC, V203, P1135
[12]   Effect of hemodialysis on leukocyte adhesion receptor expression [J].
Kaupke, CJ ;
Zhang, J ;
Cesario, T ;
Yousefi, S ;
Akeel, N ;
Vaziri, ND .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1996, 27 (02) :244-252
[13]  
Kawabata K, 1996, NEPHRON, V73, P573
[14]   DIFFERENTIAL EFFECT OF HEMODIALYSIS MEMBRANES ON HUMAN-LYMPHOCYTE NATURAL-KILLER FUNCTION [J].
KAY, NE ;
RAIJ, L .
ARTIFICIAL ORGANS, 1987, 11 (02) :165-167
[15]   Monocyte production of transforming growth factor beta in longterm hemodialysis: Modulation by hemodialysis membranes [J].
Mege, JL ;
Capo, C ;
Purgus, R ;
Olmer, M .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1996, 28 (03) :395-399
[16]   Haemodialysis monocytopenia:: differential sequestration kinetics of CD14+CD16+ and CD14++ blood monocyte subsets [J].
Nockher, WA ;
Wiemer, J ;
Scherberich, JE .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2001, 123 (01) :49-55
[17]   IDENTIFICATION AND CHARACTERIZATION OF A NOVEL MONOCYTE SUBPOPULATION IN HUMAN PERIPHERAL-BLOOD [J].
PASSLICK, B ;
FLIEGER, D ;
ZIEGLERHEITBROCK, HWL .
BLOOD, 1989, 74 (07) :2527-2534
[18]   Strong depletion of CD14+CD16+ monocytes during haemodialysis treatment [J].
Sester, U ;
Sester, M ;
Heine, G ;
Kaul, H ;
Girndt, M ;
Köhler, H .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2001, 16 (07) :1402-1408
[19]   TRAFFIC SIGNALS FOR LYMPHOCYTE RECIRCULATION AND LEUKOCYTE EMIGRATION - THE MULTISTEP PARADIGM [J].
SPRINGER, TA .
CELL, 1994, 76 (02) :301-314
[20]  
STEFONI S, 1991, NEPHROL DIAL TRANSPL, V6, P4