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Polymorphonuclear cell function and infection in dialysis.

R Vanholder¹, S Ringoir

¹Nephrology Department, University Hospital, Ghent, Belgium.

Kidney International. Supplement

|October 1, 1992

Summary

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Patients with end-stage renal disease have impaired immune function, increasing infection risk. This study reveals metabolic disturbances in immune cells, linked to uremia and dialysis, particularly affecting defense against Staphylococcus Aureus.

Area of Science:

Nephrology
Immunology
Biochemistry

Background:

End-stage renal disease (ESRD) patients exhibit heightened susceptibility to infections, a major cause of morbidity and mortality.
Phagocytic cells, crucial for bacterial defense, rely on the hexose monophosphate shunt (HMS) for metabolic support of the NAD(P)H-oxidase enzyme, which generates oxygen free radicals for pathogen destruction.

Purpose of the Study:

To investigate the functional status of the hexose monophosphate shunt (HMS) in polymorphonuclear leukocytes (PMNLs) from patients with ESRD.
To identify factors contributing to impaired immune cell function in uremia, including uremic toxicity, dialyzer membrane biocompatibility, and anemia.

Main Methods:

Measurement of CO2 production from radiolabeled glucose in whole blood samples to assess HMS activity.

Related Experiment Videos

Normalization of data based on polymorphonuclear cell counts.

Comparison of HMS function in uremic outpatients, pre-dialysis hemodialysis patients, and during dialysis with different membrane types.

Main Results:

Glycolysis is disturbed in uremic patients with serum creatinine (SCrea) ≥ 6 mg/dl and creatinine clearance (CCr) ≤ 15 ml/min.
Similar functional disturbances were observed in pre-dialysis hemodialysis patients.
Dialysis with cuprophan membranes exacerbated these functional disturbances, unlike non-complement activating dialyzers.
Immune response was particularly suppressed against Staphylococcus Aureus, a common pathogen in uremia.
Functional disturbances are attributed to uremic toxicity, dialyzer membrane bio(in)compatibility, and uremic anemia.

Conclusions:

Biochemical disturbances in PMNLs, stemming from multifactorial pathophysiological processes in ESRD, contribute to the increased incidence of infections.
Impaired HMS function compromises the ability of phagocytic cells to combat bacterial infections, especially Staphylococcus Aureus, in uremic patients.