For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
3
views
17
references
 Top references
cited by
2
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      412
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Changes of Plasma Angiotensin-Converting Enzyme Activity during Hemodialysis *

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Plasma angiotensin-converting enzyme activity was measured by spectrophotometer in normal subjects and in patients with end stage renal failure, serially during a routine hemodialysis. Patients on maintenance hemodialysis tended to be associated with elevated plasma angiotensin-converting enzyme activity versus normal subjects. Plasma angiotensin-converting enzyme activity was significantly elevated in patients with chronic renal failure after 5 hours of hemodialysis(p<.001). Plasma angiotensin-converting enzyme activity corrected for hemoconcentration was also significantly increased(p<.05). There was a significant correlation between the increase in plasma angiotensin-converting enzyme activity after 5 hours of hemodialysis and the decrease in white blood cell count at one hour of hemodialysis (r = 0.51, p<.05). It is suggested that plasma angiotensin-converting enzyme analysis may prove to be a method for assessing transient pulmonary dysfunction during hemodialysis.

          Related collections

          Most cited references17

          • Record: found
          • Abstract: found
          • Article: not found

          Elevation of serum angiotensin-converting-enzyme (ACE) level in sarcoidosis.

          Ori Lieberman (1975)
          The level of serum angiotensin-converting enzyme (ACE) was elevated in 15 of 17 patients with active sarcoidosis. Serum ACE was studied to determine the effect of chronic lung disease upon the blood level of an enzyme believed to originate from the lungs. The assay was performed in approximately 200 control subjects and 200 patients with chronic lung disease using hippuryl-L-histidyl-L-leucine as substrate. Enzyme activity greater in male control subjects than in female subjects of comparable age and greater in children than in adults. Serum ACE was significantly reduced in patients with chronic obstructive lung disease, lung cancer, tuberculosis and cystic fibrosis, as compared to control subjects, and was even lower in those receiving corticosteroids. Of greatest interest, however, was that levels in patients with active sarcoidosis not receiving steroids were greater than 2 standard deviations above the mean for the adult control subjects (greater than 11.6 units) whereas levels in patients with sarcoidosis receiving steroids and in those with resolved disease were normal. A survey of subjects with other granulomatous diseases failed to reveal any other condition that was significantly associated with a similar elevation of serum ACE levels. Elevation of ACE levels in sarcoidosis appears to be associated with the active disease process and does not appear to be a familial inherited enzyme abnormality. An assay of serum ACE is a useful tool for regulating therapy in sarcoidosis and for confirming the diagnosis, since it readily distinguishes these patients from others with tuberculosis, lung cancer or lymphoma.
          Article 0 comments Cited 61 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Complement and leukocyte-mediated pulmonary dysfunction in hemodialysis.

            P Craddock, J Fehr, K L Brigham … (1977)
            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.
            Article 0 comments Cited 44 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.

              Enrique Dalmasso, J Fehr, Barbara P. Craddock … (1977)
              Acute leukopenia occurs in all patients during the first hour of hemodialysis with cellophanemembrane equipment. This transient cytopenia specifically involves granulocytes and monocytes, cells which share plasma membrane reactivity towards activated complement components. The present studies document that complement is activated during exposure of plasma to dialyzer cellophane, and that upon reinfusion of this plasma into the venous circulation, granulocyte and monocyte entrapment in the pulmonary vasculature is induced. During early dialysis, conversion of both C3 and factor B can be demonstrated in plasma as it leaves the dialyzer. Moreover, simple incubation of human plasma with dialyzer cellophane causes conversion of C3 and factor B, accompanied by depletion of total hemolytic complement and C3 but sparing of hemolytic C1. Reinfusion of autologous, cellophane-incubated plasma into rabbits produces selective granulocytopenia and monocytopenia identical to that seen in dialyzed patients. Lungs from such animals reveal striking pulmonary vessel engorgement with granulocytes. The activated complement component(s) responsible for leukostasis has an approximate molecular weight of 7,000-20,000 daltons. Since it is generated in C2-deficient plasma and is associated with factor B conversion, it is suggested that activation of complement by dialysis is predominantly through the altermative pathway.
              Article 0 comments Cited 39 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Korean J Intern Med
                Journal ID (iso-abbrev): Korean J. Intern. Med
                Journal ID (publisher-id): KJIM
                Title: The Korean Journal of Internal Medicine
                Publisher: Korean Association of Internal Medicine
                ISSN (Print): 1226-3303
                ISSN (Electronic): 2005-6648
                Publication date (Print): January 1987
                Volume: 2
                Issue: 1
                Pages: 62-65
                Affiliations
                Department of Internal Medicine, Catholic Medical College, Seoul, Korea
                Author notes
                Address reprint requests: Wan Suh Koo, M.D., Department of Internal Medicine, Catholic Medical College, # 505 Banpodong Kangnam-Gu, Seoul, 135, Korea
                [*]

                This work was supported in part by Catholic Medical Center clinical research funds

                Article
                Publisher ID: kjim-2-1-62-10
                DOI: 10.3904/kjim.1987.2.1.62
                PMC ID: 4534915
                PubMed ID: 2856479
                SO-VID: 9a5f0595-d2ca-46cd-ad5d-1ae0a85e3193
                Copyright © Copyright © 1987 The Korean Association of Internal Medicine
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Internal medicine
                Keywords: angiotensing-converting enzyme,hemodialysis,white blood cell,pulmonary dysfunction
                Data availability:
                ScienceOpen disciplines: Internal medicine
                Keywords: angiotensing-converting enzyme, hemodialysis, white blood cell, pulmonary dysfunction

                Comments

                Comment on this article

                scite_

                Similar content412

                See all similar

                Cited by2

                See all cited by

                Most referenced authors112

                See all reference authors