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. 1982 Dec;109(3):283–287.

Alterations in activities of anaphylatoxin inactivator and chemotactic factor inactivator during hemodialysis.

J R McCormick, D L Kreutzer, H J Keating, J Hupp, A Despins, M Moore
PMCID: PMC1916121  PMID: 7180942

Abstract

The systemic infusion of complement-derived anaphylatoxin ane chemotaxins during hemodialysis results in profound transient neutropenia and may be associated with subtle pulmonary dysfunction. The fact that these potent inflammatory peptides do not usually produce serious ill effects may be due in part to their rapid inactivation by the serum regulatory proteins anaphylatoxin inactivator (AI) and chemotactic factor inactivator (CFI). Accordingly, the authors investigated the effect of hemodialysis on circulating neutrophil counts and serum levels of AI and CFI activity in 10 patients. In all patients, circulating neutrophil counts plummeted by more than 50% within 5 minutes of the onset of dialysis and rose beyond control levels by 1 hour. AI activity significantly fell from 65 +/- 16 mU/ml before dialysis to 18.7 +/- 7.8 mU/ml within 5 minutes of its initiation; levels remained depressed throughout the procedure. In contrast, CFI gradually increased, achieving a level significantly different from the predialysis value by 15 minutes. These events contrasted with the observation that activation of the complement system in vitro results in a significant decline in both CFI and AI activities. We suggest that the maintenance of or increase in CFI activity in patients undergoing hemodialysis enhances the clearance of circulating chemotactins, preventing the persistent activation of neutrophils during the procedure and subsequent organ dysfunction.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Aurigemma N. M., Feldman N. T., Gottlieb M., Ingram R. H., Jr, Lazarus J. M., Lowrie E. G. Arterial oxygenation during hemodialysis. N Engl J Med. 1977 Oct 20;297(16):871–873. doi: 10.1056/NEJM197710202971607. [DOI] [PubMed] [Google Scholar]
  2. Bokisch V. A., Müller-Eberhard H. J. Anaphylatoxin inactivator of human plasma: its isolation and characterization as a carboxypeptidase. J Clin Invest. 1970 Dec;49(12):2427–2436. doi: 10.1172/JCI106462. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Brozna J. P., Senior R. M., Kreutzer D. L., Ward P. A. Chemotactic factor inactivators of human granulocytes. J Clin Invest. 1977 Dec;60(6):1280–1288. doi: 10.1172/JCI108887. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Corbin N. C., Hugli T. E., Müller-Eberhard H. J. Serum carboxypeptidase B: a spectrophotometric assay using protamine as substrate. Anal Biochem. 1976 May 21;73(1):41–51. doi: 10.1016/0003-2697(76)90139-1. [DOI] [PubMed] [Google Scholar]
  5. Craddock P. R., Fehr J., Brigham K. L., Kronenberg R. S., Jacob H. S. Complement and leukocyte-mediated pulmonary dysfunction in hemodialysis. N Engl J Med. 1977 Apr 7;296(14):769–774. doi: 10.1056/NEJM197704072961401. [DOI] [PubMed] [Google Scholar]
  6. Dolan M. J., Whipp B. J., Davidson W. D., Weitzman R. E., Wasserman K. Hypopnea associated with acetate hemodialysis: carbon dioxide-flow-dependent ventilation. N Engl J Med. 1981 Jul 9;305(2):72–75. doi: 10.1056/NEJM198107093050204. [DOI] [PubMed] [Google Scholar]
  7. Goldblum S. E., Reed W. P. Host defenses and immunologic alterations associated with chronic hemodialysis. Ann Intern Med. 1980 Oct;93(4):597–613. doi: 10.7326/0003-4819-93-4-597. [DOI] [PubMed] [Google Scholar]
  8. Goldblum S. E., Van Epps D. E., Reed W. P. Serum inhibitor of C5 fragment-mediated polymorphonuclear leukocyte chemotaxis associated with chronic hemodialysis. J Clin Invest. 1979 Jul;64(1):255–264. doi: 10.1172/JCI109446. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Hohn D. C., Meyers A. J., Gherini S. T., Beckmann A., Markison R. E., Churg A. M. Production of acute pulmonary injury by leukocytes and activated complement. Surgery. 1980 Jul;88(1):48–58. [PubMed] [Google Scholar]
  10. Hosea S., Brown E., Hammer C., Frank M. Role of complement activation in a model of adult respiratory distress syndrome. J Clin Invest. 1980 Aug;66(2):375–382. doi: 10.1172/JCI109866. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Jacob H. S., Craddock P. R., Hammerschmidt D. E., Moldow C. F. Complement-induced granulocyte aggregation: an unsuspected mechanism of disease. N Engl J Med. 1980 Apr 3;302(14):789–794. doi: 10.1056/NEJM198004033021407. [DOI] [PubMed] [Google Scholar]
  12. Johnson K. J., Anderson T. P., Ward P. A. Suppression of immune complex-induced inflammation by the chemotactic factor inactivator. J Clin Invest. 1977 May;59(5):951–958. doi: 10.1172/JCI108717. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Kreutzer D. L., Claypool W. D., Jones M. L., Ward P. A. Isolation by hydrophobic chromatography of the chemotactic factor inactivators from human serum. Clin Immunol Immunopathol. 1979 Feb;12(2):162–176. doi: 10.1016/0090-1229(79)90005-9. [DOI] [PubMed] [Google Scholar]
  14. Kreutzer D. L., McCormick J. R., Thrall R. S., Hupp J. R., Moore V. L., Fink J. N. Elevation of serum chemotactic factor inactivator activity during acute inflammatory reactions in patients with hypersensitivity pneumonitis. Am Rev Respir Dis. 1982 May;125(5):612–614. doi: 10.1164/arrd.1982.125.5.612. [DOI] [PubMed] [Google Scholar]
  15. Lam S., Chan-Yeung M., Abboud R., Kreutzer D. Interrelationships between serum chemotactic factor inactivator, alpha 1-antitrypsin deficiency, and chronic obstructive lung disease. Am Rev Respir Dis. 1980 Mar;121(3):507–512. doi: 10.1164/arrd.1980.121.3.507. [DOI] [PubMed] [Google Scholar]
  16. Lieberman J. Carboxypeptidase B-like activity and C3 in cystic fibrosis. Am Rev Respir Dis. 1975 Jan;111(1):100–102. doi: 10.1164/arrd.1975.111.1.100. [DOI] [PubMed] [Google Scholar]
  17. Lieberman J., Nosal A., Schlessner A., Sastre-Foken A. Serum angiotensin-converting enzyme for diagnosis and therapeutic evaluation of sarcoidosis. Am Rev Respir Dis. 1979 Aug;120(2):329–335. doi: 10.1164/arrd.1979.120.2.329. [DOI] [PubMed] [Google Scholar]
  18. Patterson R. W., Nissenson A. R., Miller J., Smith R. T., Narins R. G., Sullivan S. F. Hypoxemia and pulmonary gas exchange during hemodialysis. J Appl Physiol Respir Environ Exerc Physiol. 1981 Feb;50(2):259–264. doi: 10.1152/jappl.1981.50.2.259. [DOI] [PubMed] [Google Scholar]
  19. Perez H. D., Goldstein I. M., Webster R. O., Henson P. M. Enhancement of the chemotactic activity of human C5a des Arg by an anionic polypeptide ("cochemotaxin") in normal serum and plasma. J Immunol. 1981 Feb;126(2):800–804. [PubMed] [Google Scholar]
  20. Roberts R. C., Moore V. L. Immunopathogenesis of hypersensitivity pneumonitis. Am Rev Respir Dis. 1977 Dec;116(6):1075–1090. doi: 10.1164/arrd.1977.116.6.1075. [DOI] [PubMed] [Google Scholar]
  21. Skubitz K. M., Craddock P. R. Reversal of hemodialysis granulocytopenia and pulmonary leukostasis: A clinical manifestation of selective down-regulation of granulocyte responses to C5adesarg. J Clin Invest. 1981 May;67(5):1383–1391. doi: 10.1172/JCI110166. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Ward P. A., Johnson K. J., Kreutzer D. L. Regulatory dysfunction in leukotaxis. Am J Pathol. 1977 Sep;88(3):701–710. [PMC free article] [PubMed] [Google Scholar]

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