Hemodialysis prevents liver disease caused by hepatitis C virus: Role of hepatocyte growth factor
Hemodialysis prevents liver disease caused by hepatitis C virus: Role of hepatocyte growth factor. Hemodialysis increases markedly the serum levels of hepatocyte growth factor (HGF) so that regular dialysis treatment (RDT) mimics the regular administration of HGF as a drug. Therefore, we have studie...
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Veröffentlicht in: | Kidney international 1999-12, Vol.56 (6), p.2286-2291 |
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Sprache: | eng |
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Zusammenfassung: | Hemodialysis prevents liver disease caused by hepatitis C virus: Role of hepatocyte growth factor.
Hemodialysis increases markedly the serum levels of hepatocyte growth factor (HGF) so that regular dialysis treatment (RDT) mimics the regular administration of HGF as a drug. Therefore, we have studied the effects of dialysis-associated HGF production on the severity of liver damage caused by hepatitis C virus (HCV).
Biochemical tests of liver function and liver biopsy were performed in 10 patients on RDT and in 11 patients without renal disease (WRD) converted to anti-HCV serum-positive test for the same time (48 ± 4 months). The HGF serum concentration was measured by enzyme immunoassay. In patients on RDT, HGF was measured just before starting a dialysis session (T0), at 15 and 240 minutes of dialysis (T15 and T240), and 24 hours later (T24hr).
Serum HGF was similar in WRD (average 0.17 ng/ml) as in RDT at T0 (0.25 ng/ml). In RDT serum HGF increased markedly at T15 and T240 (5.51 and 2.67 ng/ml, respectively, P < 0.001 vs. WRD and T0) and was still higher than baseline at T24hr (0.41 ng/ml, P < 0.05). Both grade of necroinflammatory activity and stage of fibrosis were significantly lower in RDT than in WRD (both, P < 0.001). The number of apoptotic hepatocytes was also significantly reduced in patients on RDT compared with patients WRD.
These results show that HCV-related liver disease is more benign in patients on RDT. The phenomenon may depend on the marked and prolonged HGF release caused by dialysis. |
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ISSN: | 0085-2538 1523-1755 |
DOI: | 10.1046/j.1523-1755.1999.00791.x |