Leukopenia, hypoxemia, and complement activation during a single hemoperfusion.

White blood cell count, acid-base balance, PO2, and complement function in five uremic patients undergoing a single hemoperfusion employing activated charcoal coated with methacrylate were studied. After 20 min on hemoperfusion, a marked leukopenia [ranging from 6,080 +/- 526 to 3,740 +/- 1,124 (p less than 0.02)] and hypoxemia [ranging from 106 +/- 13.8 to 80.2 +/- 11.9 mm Hg (p less than 0.02)] were observed. At the same time, total hemolytic complement decreased from 135 +/- 15.7 to 123 +/- 14.7 U/ml (p less than 0.001) and alternative pathway activity from 38.1 +/- 5.1 to 33.1 +/- 6.7 U/ml (p less than 0.005). C3 and B cleavage fragments were detected in the samples tested, thus demonstrating the activation of the complement alternative pathway. After 60 min, the different parameters tended to increase but did not reach the baseline levels. A direct correlation between the degree of leukopenia and the reduction of PO2 throughout the hemoperfusion period was found. pH PCO2, and HCO-3 did not change throughout the hemoperfusion period. The results demonstrate that complement activation, leukopenia, and hypoxemia occur during hemoperfusion.

[1]  E. Blackstone,et al.  Complement activation during cardiopulmonary bypass: evidence for generation of C3a and C5a anaphylatoxins. , 1981, The New England journal of medicine.

[2]  J. Bourgoignie,et al.  Leukopenia, hypoxia, and complement function with different hemodialysis membranes. , 1980, Kidney international.

[3]  H. Jacob,et al.  Effect of intravascular complement activation on granulocyte adhesiveness and distribution , 1978 .

[4]  A. Dalmasso,et al.  Complement activation and pulmonary leukotasis during nylon fiber filtration leukapheresis. , 1978, Blood.

[5]  Y. Arimoto,et al.  Inhibition of the classical and alternative pathways by amino acids and their derivatives. , 1978, Immunology.

[6]  J. Leddy,et al.  Nylon fiber leukapheresis: associated complement component changes and cranulocytopenia. , 1978, Blood.

[7]  A. Dalmasso,et al.  Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes. , 1977, The Journal of clinical investigation.

[8]  R S Kronenberg,et al.  Complement and leukocyte-mediated pulmonary dysfunction in hemodialysis. , 1977, The New England journal of medicine.

[9]  T. Platts-Mills,et al.  Activation of the alternate pathway of human complements by rabbit cells. , 1974, Journal of immunology.

[10]  Karp Rb,et al.  Changes in serum complement and immunoglobulins following cardiopulmonary bypass. , 1972 .

[11]  Haslam Pl,et al.  Complement activation during cardiopulmonary bypass , 1980 .

[12]  Cummings Rd,et al.  Role of complement activation in cell adhesion to polymer blood contact surfaces. , 1980 .

[13]  C. Ebert,et al.  Absence of cardiopulmonary dysfunction using AN-69 as compared with cellulosic membranes. , 1977, Proceedings of the Clinical Dialysis and Transplant Forum.

[14]  J. Letteri,et al.  HYPOVENTILATION AND HYPOXEMIA DURING HEMODIALYSIS: REFLEX RESPONSE TO REMOVAL OF CO2 ACROSS THE DIALYZER , 1977, Transactions - American Society for Artificial Internal Organs.

[15]  P. Fürst,et al.  THE REMOVAL OF UREMIC SMALL AND MIDDLE MOLECULES AND FREE AMINO ACIDS BY CARBON HEMOPERFUSION , 1977, Transactions - American Society for Artificial Internal Organs.

[16]  W. Briggs,et al.  RELATIONSHIP BETWEEN PULMONARY FUNCTIONS AND HEMODIALYSIS INDUCED LEUKOPENIA? , 1977, Transactions - American Society for Artificial Internal Organs.

[17]  O. S. Andersen Blood acid-base alignment nomogram. Scales for pH, pCO2 base excess of whole blood of different hemoglobin concentrations, plasma bicarbonate, and plasma total-CO2. , 1963, Scandinavian journal of clinical and laboratory investigation.

[18]  J. Scheidegger Une micro-méthode de l’immuno-électrophorèse , 1955 .