Changes in soluble ICAM-1 level during hemodialysis

K Kawabata1, Y Nagake, K Shikata

  • 1Third Department of Internal Medicine, Okayama University Medical School, Japan.

Nihon Jinzo Gakkai Shi
|November 1, 1995
PubMed

Insights

Hemodialysis increases soluble intercellular adhesion molecule-1 (sICAM-1) levels, particularly from mononuclear cells. This shedding may impair leukocyte function in patients undergoing chronic hemodialysis.

Area of Science:

  • Immunology
  • Nephrology
  • Cell Biology

Background:

  • Intercellular adhesion molecule-1 (ICAM-1) is crucial for cell interactions and is found on lymphocytes, monocytes, and endothelial cells.
  • Soluble ICAM-1 (sICAM-1) levels rise in inflammatory conditions, and leukocyte function is known to be impaired in chronic hemodialysis patients.
  • ICAM-1 can be shed from cell membranes into circulation.

Purpose of the Study:

  • To investigate the impact of hemodialysis (HD) on lymphocytes and monocytes.
  • To measure serum sICAM-1 concentrations periodically during HD.
  • To assess the relationship between HD and sICAM-1 shedding.

Main Methods:

  • Serum sICAM-1 levels were measured in chronic hemodialysis patients before and during HD sessions.
  • Levels were compared between the arterial and venous sides of the dialyzer.
  • Patients using regenerated cellulose and polymethylmethacrylate membranes were compared.

Main Results:

  • Pre-HD sICAM-1 levels were significantly elevated in patients compared to healthy subjects.
  • sICAM-1 levels increased significantly from baseline 240 minutes after HD initiation.
  • sICAM-1 levels were higher at the venous side compared to the arterial side of the dialyzer.
  • No significant difference in sICAM-1 levels was observed between the two membrane types.

Conclusions:

  • Hemodialysis stimulates the shedding of ICAM-1 from mononuclear cells (lymphocytes and monocytes).
  • The increase in sICAM-1 during HD suggests a link between the dialysis membrane and cell activation.
  • Chronic hemodialysis may compromise mononuclear cell function through ICAM-1 shedding.

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