Background. Prevalence and pathogenicity of hepatitis G virus infection in
long-term renal transplant recipients, are not fully known.
Aim. To evaluate long-term impact of HGV infection on liver disease of rena
l transplanted patients.
Patients and Methods. A total of 155 hepatitis B surface antigen negative k
idney transplant recipients, followed for a mean of 11 years after renal tr
ansplantation, were studied. Of these 48 (31%) patients had persistently el
evated serum aminotransferase values. Frozen serum samples were tested for
HGV-RNA and HCV-PNA by nested reverse transcribed polymerase chain reaction
, and for anti-hepatitis G virus and anti-hepatitis C virus by enzyme-linke
d immunosorbent assay. Hepatitis C virus-PNA was typed by a line probe assa
y and quantified by a branched DNA signal amplification assay
Results. Hepatitis G virus-PNA was detected in 37 (24%) patients and anti-h
epatitis G virus in another 26 (17%). Seventy (45%) patients had serum anti
-hepatitis C virus and 63 of these (90%) had serum hepatitis C virus-PNA. H
epatitis G virus-PNA positive and negative patients were similar in terms o
f age, sex, duration of dialysis, rate of transfusion, chronic liver diseas
e, rate of hepatitis C virus infection and immunosuppressive therapy. Fifte
en (41%) hepatitis G virus-PNA seropositive patients were hepatitis C virus
co-infected. Hepatitis C virus-PNA levels were significantly lower in the
15 hepatitis C virus/hepatitis G virus co-infected patients than in the 48
patients with hepatitis C virus infection only (2.2 vs 10.8 MEq/ml, p=0.02)
. Only 3 hepatitis G virus carriers had persistently elevated alanine amino
transferase compared to 29 hepatitis C virus carriers ( 14% vs 60%, p<0.001
), 10 patients co-infected with both hepatitis G virus and hepatitis C viru
s, and in 6 patients with neither infection (67% vs 8%, p<0.001).
Conclusions. Hepatitis G virus infection is common among kidney transplant
patients, it carries a low risk of chronic liver disease even in long-term
follow-up. Low levels of hepatitis C virus-PNA found in hepatitis G virus c
arriers suggest an interaction between these two viruses in immunosuppresse
d patients.