Ward R A, McLeish K R
Department of Medicine, School of Medicine, University of Louisville, KY 40292, USA.
J Am Soc Nephrol. 1995 Mar;5(9):1697-702. doi: 10.1681/ASN.V591697.
Previous reports that polymorphonuclear leukocyte (PMN) function is impaired in hemodialysis patients do not differentiate between effects of dialysis and of uremia. The hypothesis that chronic renal insufficiency impairs PMN function was tested. Phagocytosis and oxidative burst were measured in PMN from patients with varying degrees of chronic renal insufficiency impairs PMN function was tested. Phagocytosis and oxidative burst were measured in PMN from patients with varying degrees of chronic renal insufficiency (creatinine clearance, 6 to 35 mL/min per 1.73 m2) and normal subjects. The ability of tumor necrosis factor-alpha (TNF-alpha) to prime the oxidative burst was also assessed. Phagocytosis of Staphylococcus aureus and basal H2O2 and O2- release by PMN did not differ between normal subjects and patients with chronic renal insufficiency. However, the oxidative burst stimulated by S. aureus and formyl-Met-Leu-Phe, but not phorbol myristate acetate, was significantly enhanced in PMN from patients with chronic renal insufficiency. The increase in formyl-Met-Leu-Phe-stimulated oxidative burst correlated significantly with the level of renal function. TNF-alpha significantly increased S. aureus-induced H2O2 production in normal PMN, but not in PMN from patients with chronic renal insufficiency. These data indicate that chronic renal insufficiency does not impair PMN phagocytosis and oxidative burst. To the contrary, it enhances receptor-mediated oxidative burst. The inability of TNF-alpha to further enhance the oxidative burst suggests that PMN exist in a primed state in patients with chronic renal insufficiency.
