Complement activation during exposure of plasma to
cuprophan has been postulated to cause
leukopenia and
hypoxia in
hemodialysis patients. To determine if
hypoxia is related to
leukopenia and if complement activation leads to a depletion of functional
complement components, we dialyzed four patients three times sequentially against each of four types of membranes:
cuprophan,
regenerated cellulose,
cellulose acetate, and polyacrilonitrile. Within 20 min there was a marked
leukopenia with
cuprophan from 5541 +/- 376 to 1216 +/- 94 (P less than 0.001) and with
regenerated cellulose from 5541 +/- 411 to 1533 +/- 203 (P less than 0.001). With
cellulose acetate, the change from 5558 +/- 400 to 3783 +/- 341 (P less than 0.001) was less dramatic, and with polyacrilonitrile the fall from 5591 +/- 381 to 464 +/- 401 (P less than 0.02) was minimal. After 2 and 4 hours of dialysis, a rebound
leukocytosis was seen with
cuprophan,
regenerated cellulose, and
cellulose acetate, but not with polyacrilonitrile. Transient
thrombocytopenia occurred with
cuprophan and
regenerated cellulose. In spite of the variable degree of
leukopenia, all membranes induced a similar and significant
hypoxia, which was progressive throughout dialysis, even during the rebound
leukocytosis. After 4 hours, the mean PO2 ranged from 91 to 93 mm Hg with all membranes. Functional hemolytic titers of whole
complement, C3, C5, and C4 were normal prior to
hemodialysis and failed to decrease after 4 hours with any membrane. It is concluded that
hemodialysis leukopenia is membrane-dependent and is not the cause of
hypoxia. In addition,
hemodialysis complement activation does not lead to functional
complement depletion and is of no clinical significance.