Complement and Leukocyte-Mediated Pulmonary Dysfunction in Hemodialysis

TLDR

Cardiopulmonary decompensation during hemodialysis may result from leukocyte plugging of pulmonary vessels. Leukopenia during hemodialysis, associated with impaired pulmonary function, is driven by complement‑mediated leukostasis, as demonstrated in animal models and prevented by complement preinactivation.

Abstract

During hemodialysis, cardiopulmonary decompensation may appear in uremic patients, possibly caused by plugging of pulmonary vessels by leukocytes. In 34 patients we noted leukopenia (20% of initial levels) during hemodialysis that in 15 was associated with impaired pulmonary function. When we infused autologous plasma, incubated with dialyzer cellophane, into rabbits and sheep, sudden leukopenia and hypoxia occurred, with doubling of pulmonary-artery pressures and quintupling of pulmonary-lymph effluent. Histologic examination showed severe pulmonary-vessel-leukostasis and interstitial edema. The syndrome was prevented by preinactivation of complement but was reproduced by infusions of plasma in which complement was activated by zymosan. Thus, acute pulmonary dysfunction from complement-mediated leukostasis may play a major part in the acute cardiopulmonary complications of cellophane-membrane hemodialysis.