Impact of hepatitis C virus infection on neutrophil oxidative burst function in hemodialysis patients.

Polymorphonuclear leukocyte (PMN) functions have been studied extensively in hemodialysis (HD) patients; however, results are contradictory and the mechanisms that modulate phagocytosis and oxidative burst are not completely understood. Hepatitis C virus (HCV) is a frequent complication of HD that may be associated with disturbed PMN function; however, the impact of HCV infection on neutrophil oxidative burst function in HD patients is unknown. We investigated Neutrophil oxidative burst function in 24 HD patients (15 HCV-positive and, 9 HCV-negative patients) before and after dialysis. HCV-RNA was detected by RT-nested PCR while, quantitative measurement of oxidative burst function was assessed by flowcytometry. Neutrophil Oxidised burst function was significantly diminished in HD patients as comapred to controls (P = 0.001, oxidised PMN (%); P = 0.02 mean flueresnce intensity, MFI), and in pre-dialysis as compared to post-dialysis samples (oxidised PMNs (%): 60.5 +/- 3.2 vs. 72.1 +/- 3.9, P = 0.02); (MFI: 352 +/- 42 vs. 500 +/- 50, P = 0.03). Alteration in Neutrophil oxidative burst function in the pre-dialysis samples was significant in HCV-positive patients as compared to HCV-negative patients (oxidized PMNs (%): 50 +/- 2.9 vs. 63 +/- 5.1, P = 0.02); (MFI: 291 +/- 31 vs. 438 +/- 64, P = 0.006). Marked reduction in E. coli induced burst in pre-dialysis samples compared to post-dialysis was found in HCV-positive when compared to HCV-negative patients (oxidized PMNs (%): 50 +/- 2.9 vs. 74.8 +/- 4.7, P = 0.001), (MFI: 291 +/- 31 vs. 493 +/- 63, P = 0.002). In conclusion, a possible role of concomitant HCV infection in alteration of Neutrophil oxidative burst function is highly suggested.