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 per cent 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. (N Engl J Med 296:769–774, 1977) Transient leukopenia, selectively involving granulocytes and monocytes, occurs in all patients during the first two hours of hemodialysis with cellophane-membrane apparatus.12 We recently reported that such leukopenia results from pulmonary sequestration of leukocytes, somehow provoked by low-molecular-weight (7000 to 20,000 daltons) complement component (or components), which, in turn, were shown to be activated by dialyzer cellophane.34 Thus, immunoelectrophoretic analysis of plasma from dialyzed patients revealed conversion of both C3 and factor B during the first hour of each dialysis, and simple incubation of human plasma with cellophane from a dialyzer caused identical complement activation. Moreover, infusions of cellophane-exposed, autologous plasma.