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Dysfunction of polymorphonuclear leukocytes in uremia

M Haag-Weber1, W H Hörl

  • 1Department of Medicine, University of Vienna, Austria.

Seminars in Nephrology
|May 1, 1996
PubMed
Summary
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Uremic patients have impaired polymorphonuclear leukocyte (PMNL) function, increasing infection risk. Uremic toxins and dialysis treatments further compromise PMNLs, but therapies targeting calcium and inhibitory compounds show promise.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Uremic patients exhibit increased infectious complications due to impaired cellular host defense.
  • Polymorphonuclear leukocytes (PMNLs) in uremia show metabolic and functional abnormalities, including altered adherence, oxidative burst, chemotaxis, and phagocytosis.
  • Elevated cytosolic calcium and chronic hemodialysis with bioincompatible membranes contribute to PMNL dysfunction.

Purpose of the Study:

  • To summarize the known impairments in polymorphonuclear leukocyte (PMNL) function in uremic patients.
  • To identify factors contributing to PMNL dysfunction in chronic renal failure and during hemodialysis.
  • To review inhibitory compounds found in uremic serum that affect PMNL activity.

Main Methods:

  • Review of existing literature on PMNL function in uremia.

Related Experiment Videos

  • Analysis of studies correlating PMNL dysfunction with ferritin and cytosolic calcium levels.
  • Identification and characterization of granulocyte inhibitory compounds in uremic serum.

    • Main Results:

    • PMNL dysfunction in uremia involves altered adherence, oxidative burst, chemotaxis, phagocytosis, and intracellular killing.
    • Increased cytosolic calcium and hemodialysis trigger neutrophil activation and chronic downregulation of phagocyte function.
    • Uremic serum contains inhibitory compounds like p-cresol, granulocyte inhibitory proteins, and immunoglobulin light chains that depress PMNL function.

    Conclusions:

    • Uremia significantly impairs PMNL function, increasing susceptibility to infections.
    • Therapeutic strategies normalizing cytosolic calcium or blocking inhibitory pathways may improve PMNL function.
    • Understanding uremic toxins and inhibitory peptides is crucial for developing interventions against infectious complications.