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Peritoneal dialysis fluid inhibition of phagocyte function
Author(s) -
Tomasz Liberek,
Nicholas Topley,
Achim Jörres,
Gerald A. Coles,
Gerhard M. Gahl,
J D Williams
Publication year - 1993
Publication title -
journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.451
H-Index - 279
eISSN - 1533-3450
pISSN - 1046-6673
DOI - 10.1681/asn.v381508
Subject(s) - lactate dehydrogenase , endocrinology , peritoneal dialysis , medicine , zymosan , chemistry , phagocytosis , respiratory burst , biochemistry , biology , immunology , enzyme , in vitro
Solutions were formulated to examine, independently, the roles of osmolality and glucose in the reduction of viability and inhibition of phagocyte function by dextrose-containing peritoneal dialysis fluids. The exposure of neutrophils (polymorphonuclear leukocytes) to test fluids containing > or = 2.7% (wt/vol) glucose resulted in significant cytotoxicity as assessed by the release of lactate dehydrogenase above control values (7.12 +/- 2.65%). At the highest concentration of glucose (4.5%), lactate dehydrogenase release was 15.83 +/- 0.49% (P < 0.05). These effects were directly related to the presence of D-glucose in the test fluids. In contrast, phagocytosis and the release of leukotriene B4 from PMN stimulated with serum-treated zymosan were significantly inhibited in an osmolality-, but not glucose-, dependent manner. The inhibition of tumor necrosis factor alpha and interleukin-6 release from mononuclear leukocytes was inhibited by a combination of osmolality and monosaccharide concentration. Under the same conditions, PMN respiratory burst activation remained unaffected irrespective of glucose concentration or fluid osmolality. These data indicate that, in addition to the low pH of peritoneal dialysis fluid and its high lactate concentration, its glucose content (either directly or as a consequence of the resulting hyperosmolality of the fluid) inhibits cell functional parameters. These findings suggest clinically significant inhibition of host defense mechanisms because, in high-glucose dialysis fluids, osmolality does not reach physiologic values, even during extended intraperitoneal dwell periods.

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