Transplantation, not dialysis, corrects azotemia-dependent priming of the neutrophil oxidative burst.

Abstract

The oxidative burst of neutrophils from patients with renal failure before the initiation of dialysis is primed for an enhanced response after stimulation by phagocytosis or chemoattractants. This study shows that phagocytosis-stimulated oxidative burst activity remains primed in patients treated with both high-efficiency hemodialysis and continuous ambulatory peritoneal dialysis (CAPD), but it is normal in patients with a functioning renal transplant. Incubation of normal neutrophils or HL-60 granulocytes in azotemic plasma results in increased resting and phagocytosis-stimulated H2O2 production, which is rapidly reversible on removal of the plasma. Priming of the oxidative burst by azotemic plasma is independent of changes in opsonization and phagocytosis and does not require protein synthesis. These results suggest that azotemic plasma contains a substance or substances capable of reversibly priming oxidative burst activity in neutrophils and neutrophil-like cell lines. The Inability of high-efficiency hemodialysis and CAPD to normalize oxidative burst activity suggests that this substance is of higher molecular weight.