Cuprophane 투석막이 혈장보체 활성화와 B2-microglobulin제거율에 미치는 영향

• Published in: Kidney research and clinical practice Vol. 13; no. 3; pp. 489 - 497
• Main Authors: 배장호, 박근용, 박성배, 김현철
• Format: Journal Article
• Language: Korean
• Published: 대한신장학회 01.09.1994
• ISSN: 2211-9132

It has long been known that complement activation plays a pivotal role in the pathogensis of hemodialysis- induced leukopenia through the release of anaphylatoxins, C3a and Csa. Efficient removal of B- microglobulin in end-stage renal failure patients is a continuing preoccupation, as the incidence and severity of dialysis-associated amyloidosis are increasing. The present study was conducted to evaluate both the biocompatibility profile and the capacity to remove pa- microglobulin during hemodialysis using a cuprophane membrane. In this study, plasma C3a, C5a, leukocytes counts, and serum g-microglobulin were measured in 10 stable patients with chronic renal failure, undergoing mainte- nance hemodiaiysis with cuprophane membrane. The plasma levels of C3a desArg were significantly elevated at the first 15 minutes after initation of hemodialysis, and then slowly returned to basal level at 4 hours. However, the plasma levels of C5a desArg did not show any significant change during hemodialysis. Leukocyte counts decreased significantly from 6396±1811/mm' before dialysis to 1986±742/mm at 15 minutes after initiation of hemodialysis (p<0.0005), and almost retured to predialysis values at 60 minutes after dialysis. There was a significant correlation between leukocyte counts and plasma C3a desArg levels at the first 15 minutes after initiation of hemodialysis (r=0.81, p<0. 005) and during hemodialysis (r =0.32, p <0.05). Our study showed a 3.3% increase of serum B-microglobulin after correction for hemoconcetration during hemodialysis. In conclusion, the present study showed that this cuprophane menbrane displays a bad profile of biocompatibility as well as a bad capacity to remove B- microglobulin when used in dialysis. Therefore other therapeutic alternatives have to be designed to prevent dialysis induced hypoxemia and B-microglobulin amyloidosis.