Effect of hemodialysis schedules and membranes on hepatocyte growth factor and hepatitis C virus RNA levels
✍ Scribed by Guillermina Barril; Javier Bartolomé; Paloma Sanz; Emmanuela Buoncristiani; Juan Antonio Traver; Rafael Selgas; Umberto Buoncristiani; Inmaculada Castillo; Juan Antonio Quiroga; Vicente Carreño
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 76 KB
- Volume
- 82
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Hemodialysis induces production of the hepatocyte growth factor (HGF) and decrease of serum hepatitis C virus (HCV) RNA in patients with HCV infection, but it is not known if the hemodialysis schedule or type of membrane affect both the HGF production and HCV viremia. The effects on both parameters of alternate‐day intermittent hemodialysis and short‐daily hemodialysis and high and low flux membranes were investigated in 41 patients treated by hemodialysis. Sixteen (39%) patients were anti‐HCV positive and 11 (69%) had HCV RNA. Twenty‐six patients were on alternate‐day intermittent and 15 on short‐daily hemodialysis. High flux membranes were used for 29 patients and low flux membranes for 12 patients. A decrease in HCV RNA was observed at the end of hemodialysis (8.6 × 10^5^ ± 1.1 × 10^6^ IU/ml vs. 4.4 × 10^5^ ± 7.3 × 10^5^ IU/ml, P = 0.003). The proportion of HCV RNA decrease was similar in patients dialyzed with both schedules and with both types of membranes. The HGF levels increased from 2,605.9 ± 1,428.7 to >8,000 pg/ml at 15 min. At the end of the session, the HGF levels decreased to 5,106.7 ± 2,533.9 pg/ml. The HGF levels at the start of the next session were similar to those at baseline (2,680.0 ± 1,209.3 pg/ml). The increase and dynamics of the HGF levels were similar in patient's hemodialyzed with both schedules and with both types of membranes. These results suggest that changes in HCV RNA and HGF levels during hemodialysis are not influenced by the schedule or type of membrane used. J. Med. Virol. 82: 763–767, 2010. © 2010 Wiley‐Liss, Inc.
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