Histological evolution of hepatitis C virus
infection after renal transplantation
Uehara SNO, Emori CT, Pereira PSF, Perez RM, Medina Pestana JO,
Lanzoni VP, Silva ISS, Silva AEB, Ferraz MLCG. Histological evolution
of hepatitis C virus infection after renal transplantation.
Abstract: Background: information regarding histological progression of
hepatitis C after renal transplant (RTx) is scarce.
Aims: To analyze clinical and laboratory evolution and histological
progression of hepatitis C in patients evaluated before and after RTx.
Methods: Twenty-two HCV-infected patients submitted to liver biopsy
pre- and post-RTx were included. A semiquantitative analysis of
necroinflammatory activity and fibrosis staging was performed and the
two biopsies were compared.
Results: Patients were mostly men (73%) with mean age of 36 ± 9 yr.
Time post-transplant was 4 ± 2 yr and time between biopsies was
5 ± 2 yr. An elevation of alanine aminotransferase (p = 0.041) and
aspartate aminotransferase (p = 0.004) levels was observed in the post-
transplant period. Fibrosis progression after renal transplantation was
observed in 11 (50%) of the patients, and necroinflammatory activity
worsening was observed in 7 (32%) of the patients. The histological
progression occurred even among those without significant histological
lesions in pre-transplant biopsy.
Conclusion: The findings of this study suggest that the practice of
indicating treatment in the pre-transplant phase based mainly on
histological disease should be revised, because a high proportion of
patients present disease progression. Because interferon cannot be used
safely after RTx, treatment should be indicated for all ESRD patients
with hepatitis C.
Silvia Naomi de Oliveira Ueharaa,
Christini Takemi Emoria, Patrı ´cia
da Silva Fucuta Pereiraa, Renata
M. Perezb, Jose ´ Osmar Medina
Pestanac, Vale ´ria Pereira
Lanzonid, Ivonete Sandra Souza e
Silvaa, Antonio Eduardo Benedito
Silvaaand Maria Lucia Cardoso
aDivision of Gastroenterology, Universidade
Federal de Sa ˜o Paulo,bDivision of Hepatology,
Universidade Federal do Rio de Janeiro,
cDivision of Nephrology, Universidade Federal
do Rio de Janeiro, anddDepartment of
Pathology, Universidade Federal do Rio de
Key words: chronic kidney failure –
hemodialysis – hepatitis C – kidney
transplantation – liver disease
Corresponding author: Silvia Naomi de
Oliveira Uehara, Rua 9 de julho, 1408 – Vila
Ipiranga – Campo Grande, Mato Grosso do
Sul - CEP: 79081-050, Brazil.
Tel.: 55 67 9994 3637; fax: 55 67 3345 3651
Conflict of interest: The authors declare that
they do not have any conflict of interest. This
study has been supported by the Brazilian
National Council for Scientific and
Technological Development (CNPq).
Accepted for publication 17 January 2012
Hepatitis C virus (HCV) infection is of great
importance among end-stage renal disease (ESRD)
and renal transplant patients, not only for its high
prevalence when compared to the general popula-
tion but also because of its impact on patient and
renal graft survival.
Chronic hepatitis C has a distinct natural his-
tory in ESRD population when compared to the
characteristics, there is no correlation between
alanine aminotransferase (ALT) levels, viral load,
and histological findings (1, 2). Therefore, liver
biopsy is considered the most accurate assess-
ment of the severity of the liver disease and
could be a predictor of its evolution post-
Several studies have shown that patients with
ESRD have less severe histological lesions than
non-uremic patients, although the reason for this
difference is not fully understood (6–9). However,
modifications in disease evolution can occur after
renal transplantation, and the outcomes are largely
The histological progression of hepatitis C in
post-renal transplant patients is controversial, with
cross-sectional studies in distinct patient groups
© 2012 John Wiley & Sons A/S
Clin Transplant 2012 DOI: 10.1111/j.1399-0012.2012.01635.x
showing more aggressive disease in renal trans-
plant patients when compared to patients with
ESRD, while others have observed no significant
differences (7, 10).
During the post-renal transplant phase, studies
evaluating serial biopsies are scarce. Rao et al.
observed hepatic disease progression in 60% of
patients with an initial biopsy showing mild
chronic active hepatitis and in 100% of patients
with intense chronic active hepatitis. From the data
obtained, it was concluded that histological diag-
nosis could be a useful marker to predict the course
of hepatic disease after renal transplantation (4).
Alric et al. have also evaluated the impact of
renal transplant in the histological liver disease
and observed that the progression of fibrosis
between two hepatic biopsies after the transplant is
slow in renal transplant patients when compared
to immunocompetent (9).
Longitudinal data related to clinical outcomes,
histological progression, and potential treatment
impact in the same group of patients evaluated in
pre- and post-renal transplant phases are very
scarce. The aim of this study was to evaluate the
histological evolution of hepatitis C after renal
pre- and post-transplant liver biopsies. This infor-
mation could be very useful to establish the best
selection criteria for hepatitis C treatment during
the pre-transplant period.
Patients and methods
The study included 22 renal transplant patients
with chronic HCV infection who underwent a pre-
transplant evaluation at the Hepatitis Outpatient
Clinic of the Federal University of Sao Paulo from
August 1998 to December 2008. Our hospital is a
reference center for pre-renal transplant patients
with HCV infection, who are referred from differ-
ent hemodialysis units.
defined by qualitative positive HCV-RNA, hepatic
biopsies pre- and post-renal transplant with ade-
quate fragments, and time since transplant greater
than six months were included. Patients with con-
comitant hepatitis B virus (HBV) and human
immunodeficiency virus (HIV) infection were
excluded. We also excluded those who consumed
more than 20 g of alcohol per day and those with
other causes of liver disease. Patients were
evaluated for clinical, laboratory, and histological
progression post-transplant. This study protocol
was submitted to the local ethics committee and
followed all of the ethical premises of the Helsinki
Declaration, revised in 2000.
Demographic, epidemiological, and clinical data
The following variables were analyzed: age at the
time of renal transplant; gender; baseline renal dis-
ease; duration of infection (estimated by the initial
date of hemodialysis, or first blood transfusion if
occurring before 1992); time on hemodialysis; time
since renal transplant; time between the pre-trans-
plant biopsy and transplant; time between the two
biopsies (pre- and post-transplant); time between
transplant and the second biopsy; type of donor
(living or non-living donor); immunosuppressive
regimen; previous renal transplant history; post-
transplant outcome (abandonment, graft rejection,
and death); and history of previous HCV treat-
Serum levels of ALT, aspartate aminotransferase
(AST), gamma-glutamyltransferase (GGT), total
bilirubin (BT), prothrombin activity (PA), and
albumin were analyzed by automated methods at
the time of the pre- and post-transplant liver biop-
sies. The liver enzymes ALT, AST, and GGT were
expressed as times the upper limit of normal
Serological and molecular tests
The anti-HCV antibody analysis was performed
with a third generation immunoenzymatic method
using core antigens in the NS3 and NS4 regions
(anti-HCV; Abbott Laboratories, Chicago, IL,
USA), and the HCV-RNA was investigated by
detection (Cobas Amplicor HCV Test; Roche
Diagnostic Systems, Indianapolis, IN, USA).
a 50 IU/mLlimit of
Liver tissue samples were obtained by Tru-Cut
needle biopsy. In the pre-transplant period, liver
biopsy was indicated for all patients with evidence
of viral replication (qualitative HCV-RNA PCR
positive) independent of ALT levels. In the post-
transplant phase, liver biopsy was indicated for
patients with ALT elevation, infection duration
greater than ten yr or time after transplant greater
than five yr.
A single pathologist blinded to the patient clini-
cal data analyzed all biopsies. Analysis of fibrosis
Uehara et al.
based on the semiquantitative criteria proposed by
Ludwig (11) and Desmet et al. (12) for the classifi-
cation of chronic HCV infection. For comparative
analysis, the variables were categorized according
to improvement/stability versus worsening of sep-
tal fibrosis and interface hepatitis.
Numerical variables were expressed as means and
standard deviations, and categorical variables were
expressed as percentages of the total. Categorical
variables were statistically compared using the chi-
square (v2) and Fisher’s exact tests, when neces-
sary. The Wilcoxon test was used for numerical
variable comparison in the same patient group
between pre- and post-transplant samples. A p
value of less than 0.05 (a = 5%) was considered
From 537 patients evaluated with ESRD and
chronic HCV infection during pre-transplant per-
iod, 309 patients underwent a liver biopsy. Among
these patients, 66 underwent renal transplantation
and 22 who were submitted to a post-renal trans-
plant liver biopsy were included in the study.
Descriptive analysis of the renal transplant patients
Patients were mostly men (73%), with an average
age at the time of transplant of 36 ± 9 yr. Renal
disease was attributed to glomerulonephritis in
41% of the cases and to systemic arterial hyperten-
sion in 18% of the cases. The duration of hemodi-
alysis was 6 ± 3 yr, and the time of infection was
9 ± 7 yr. Renal grafts were from living donors in
59% of the cases. Only seven (32%) of the patients
underwent pre-transplant HCV treatment, and five
(23%) had previous renal transplantation. The
most widely used immunosuppressive regimen
included mycophenolate mofetil in 59% of cases,
tacrolimus in 32%, cyclosporine in 27%, and aza-
thioprine in 18% of cases.
Laboratory evolution and histological progression of
patients who underwent hepatic biopsy before and
after renal transplantation (n = 22)
The time between the pre-transplant biopsy and
transplantation was 1 ± 1 yr. The interval between
the two biopsies (pre- and post-transplant) was
5 ± 2 yr, and the time between transplantation
and the second biopsy was 4 ± 2 yr. The compara-
tive analysis of laboratory parameters at the time
of the pre- and post-transplantation biopsies is
shown in Table 1.
The histological progression of the pre- and
post-renal transplant liver biopsies is shown in
Tables 2 and 3. With regard to staging, fibrosis
worsened in 11 patients (50%) and was stable or
improved post-transplant in 11 patients (50%).
Considering only the cases with persistently nor-
mal ALT (n = 12), we observe a progression of
liver fibrosis in 50%. The periportal/septal necroin-
flammatory activity worsened in seven (32%) of
the patients and remained stable or improved in
15. Table 4 describes how many patients had both
fibrosis and necroinflammatory changes vs. those
with fibrosis or necroinflammatory activity pro-
Table 1. ALT, AST, GGT, total bilirubin, albumin, and PA levels at
the time of the pre- and post-renal transplantation liver biopsies
ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT,
gamma glutamyltransferase; BT, total bilirubin; PA, prothrombin activity.
Table 2. Fibrosis staging in pre- and post-renal transplant biopsies
(n = 22)
Fibrosis staging post-RTx
Fibrosis staging pre-RTx0
RTx, renal transplantation.
Table 3. Periportal/septal necroinflammatory activity (PPA) in pre-
and post-renal transplant liver biopsies (n = 22)
PPA in biopsy post-RTx
PPA in biopsy
PPA, periportal/septal necroinflammatory activity; RTx = renal transplan-
Hepatitis C: evolution post-renal transplantation
Ten patients (45%) were submitted to a liver
biopsy based on ALT elevation. In the compara-
tive analysis of ALT levels at the moment of
post-transplant liver biopsy, no difference was
observed between the groups with and without
histological progression (p = 0.751), indicating
that the finding of disease progression in this
sample was probably not related to a bias in the
selection of patients to the liver biopsy.
In patients with histological progression (fibrosis
and/or necroinflammatory activity), AST signifi-
cantly raised comparing pre- and post-transplant
determination (p = 0.007) and ALT showed also a
tendency of elevation (p = 0.09). On the other
hand, in patients without histological progression,
there was no difference in pre- and post-transplant
ALT (p = 0.17) and AST (p = 0.35) determina-
tions. The mean post-transplant time in the group
with histological progression was 4.9 ± 1.8 yr,
while in the group without histological progres-
sion, the mean was 3.5 ± 2.4 yr (p = 0.06).
Histological progression of untreated patients who
biopsies (n = 15)
A specific analysis of patients who had not
undergone previous treatment was conducted to
evaluate the natural course of HCV infection after
renal transplant without any influence of HCV
treatment prior to the transplant. The histological
evolution of the 15 untreated patients can be found
in Tables 5 and 6. Nine (60%) cases worsened
fibrosis staging, and the periportal/septal necroin-
flammatory activity (interface hepatitis) increased
in 5 (33%).
Comparison of histological progression between
treated and untreated HCV patients in the pre-renal
Among the patients who underwent serial biopsies
(n = 22), only seven received pre-renal transplant
HCV treatment. Of these, two showed fibrosis
stage worsening and five showed maintenance or
an improvement in fibrosis.
A comparative analysis of the histological evolu-
tion between treated and untreated patients in the
pre-transplant period demonstrated that there was
no difference in the worsening of periportal/septal
activity between treated and untreated patients
(29% vs. 33%; p = 0.61). Conversely, we observed
worsening of fibrosis in two of the seven (29%)
treated patients and nine of the 15 (60%) untreated
patients (p = 0.18). This difference did not reach
statistical significance probably due to the small
Only one patient lost the renal graft, and the cause
was defined as membranoproliferative glomerulo-
nephritis (MPGN). Three patients died because of
infection, lymphoproliferative disease, and liver
failure accompanied by variceal gastrointestinal
This study aimed at assessing the clinical, labora-
tory, and histological evolution of hepatitis C in
renal transplant patients who underwent pre- and
Table 4. Fibrosis and periportal/septal necroinflammatory activity
(PPA) evolution in post-renal transplant liver biopsies (n = 22)
or stability (%) Worsening (%)
Improvement or stability
PPA, periportal/septal necroinflammatory activity.
Table 5. Fibrosis staging of pre- and post-renal transplant liver biop-
sies in previously untreated patients (n = 15)
Fibrosis staging post-RTx
RTx, renal transplant.
Table 6. Periportal/septal necroinflammatory activity (PPA) in pre-
and post-renal transplant biopsies in previously untreated patients
(n = 15)
PPA in biopsy post-RTx
PPA in biopsy
PPA, periportal/septal necroinflammatory activity; RTx, renal transplant.
Uehara et al.
post-renal transplant liver biopsies. Understanding
HCV evolution post-transplant is critical to estab-
lishing treatment strategies before renal transplan-
approaches have been based mainly on histological
findings. However, it has not been investigated the
pattern of histological progression after the renal
transplant in patients with mild histological lesions
in the pre-transplant period. If this progression
occurs, the management of patients eligible for
transplantation should be revised because post-
transplant treatment has important limitations.
To date, the available data on the histological
progression of hepatitis C in the same patient using
histological biopsy findings pre- and post-trans-
plant are scarce, because of the difficulty in per-
forming longitudinal studies in this population (13,
14). There are difficulties in obtaining a significant
number of individuals because of the small number
of renal transplants in relation to the number of
patients with ESRD on the waiting list and because
this population has high rates of morbidity and
mortality because of associated diseases (15–17).
After the transplant, there is also a great risk of
graft loss, bringing additional limitation for the
reassessment of liver disease. Therefore, cross-sec-
tional studies that compare distinct patient groups
(ESRD and renal transplant patients) are more fre-
quent, but remain controversial on demonstrating
whether there is or not histological progression of
the disease after renal transplantation (7, 10, 18).
In this study, the goal was to evaluate a retro-
spective cohort of 22 renal transplant patients by
following the laboratory evolution and histological
progression of the hepatitis C as well as the clinical
outcome. The included patients had undergone a
routine protocol of liver biopsies pre- and post-
transplant, with an interval of 5 ± 2 yr.
During the follow-up period of this study, three
patients died: one because of infection, one because
of lymphoproliferative disease, and one from liver
failure. These findings are consistent with the liter-
ature, which reports a higher incidence of deaths
for these specific reasons among renal transplant
patients with chronic HCV infection when com-
pared to non-infected (2, 19–22). There was one
graft loss because of MPGN, which was confirmed
by renal histological studies. HCV may be the pri-
mary cause of renal disease usually associated with
cryoglobulinemia and MPGN, which may lead to
graft loss (23).
Regarding the laboratory evolution, ALT and
AST showed a significant elevation in the post-
transplant period. This may be due to a worsening
of histological lesions after transplantation or to
the hepatotoxic effects of immunosuppressive
drugs. Additionally, it could be caused by the loss
of the mechanisms related to the reduction in
serum levels of hepatic enzymes that occur in he-
modialysis patients (24, 25). The other laboratory
parameters examined showed no significant altera-
tions pre- and post-transplant, indicating that liver
function did not worsened during this time period.
Regarding histological progression after renal
transplant, which represents the main objective of
this study, we observed that fibrosis worsened
when comparing pre- and post-renal transplanta-
tion liver biopsies in 50% of the patients. In addi-
tion, necroinflammatory activity worsened in 32%
of the patients. Four patients (18%) showed com-
bined progression of both fibrosis and necroinflam-
matory activity, while in 7 (32%), only the fibrosis
progressed and in 3 (14%), only the necroinflam-
matory activity showed progression.
To date, only two studies have described the his-
tological evolution of HCV infection from pre- to
post-transplant in the same patient (13, 14). The
study of Gu ¨ rsoy et al. longitudinally evaluated 12
patients who were re-biopsied after 3.2 ± 2 yr of
renal transplant. Of the 12 patients, six were trea-
ted for HCV prior to renal transplant. There was
no significant difference in the Knodell score when
the pre- and post-transplant biopsies of the six
untreated patients were compared (7 ± 3.2 vs.
7.5 ± 2.1) (13).
Huraib et al. evaluated 21 renal transplant
patients, of whom 11 were treated prior to the
transplant. The 10 untreated patients showed a sta-
tistically significant increase in histological activity
index post-transplant (3.9 ± 1.2 vs. 5.5 ± 1.32;
p = 0.01) (14).
The present study does differ from these only
two previous studies in the literature. The interval
between biopsies was heterogeneous, with an inter-
val between biopsies of 5 ± 2 yr in our study,
3.2 ± 2 yr in the Gursoy study, and an undefined
interval in the Huraib study. In addition, the other
studies used the Knodell classification, which eval-
uates the combination of fibrosis and necroinflam-
matory activity, while the present study analyzed
each of these histological compartments sepa-
rately. Another important difference was the
method of statistical analysis. Both previous stud-
ies evaluated histological progression by compar-
ing the average Knodell score pre- and post-
transplant, considering the group as a whole. The
present study analyzed the progression of each
patient individually, allowing the identification of
the proportion of patients presenting histological
progression after transplantation. Therefore, it was
possible to observe that significant histological
worsening occurs in a high proportion of patients,
Hepatitis C: evolution post-renal transplantation
including those with mild histological liver disease
in pre-transplant biopsies.
The present study also evaluated the effect of
treatment and demonstrated that fibrosis worsened
in 29% of the seven treated cases and in 60% of
the untreated cases (p = 0.18). This difference was
clinically relevant; however, it was not statistically
significant, probably due to the small sample size.
In contrast to the other studies, a biopsy was not
performed after treatment in the pre-transplant
phase in the present study, once evaluating the
treatment’s histological impact was not the objec-
tive of this study. The other studies performed
these biopsies and showed histological benefits
after treatment in the pre-transplant period, with
remained after renal transplantation (13, 14).
To rule out the possible influence of treatment
on disease progression in post-renal transplant
patients, we performed a stratified analysis of 15
untreated patients. These patients were found to
have similar histological disease progression than
the group as a whole (60% fibrosis progression
and 33% necroinflammatory activity progression).
Until now, the treatment of hepatitis C in
patients with ESRD has been indicated mainly
based on histological findings, and treatment is
only recommended for patients with significant
necroinflammatory activity and/or fibrosis. The
findings of this study suggest that this practice
should be revised because patients with mild
histological liver disease may present disease
progression and even death as a result of liver
failure. Because interferon cannot be used safely
after the renal transplantation, treatment should
be indicated for all ESRD patients with hepatitis C
in the pre-transplant period.
Silvia Naomi de Oliveira Uehara contributed to
concept, design, data collection and analysis, statis-
tics, interpretation, and drafting the article; Chris-
tini Takemi Emori was involved in data collection
and analysis; Patrı´cia da Silva Fucuta Pereira was
involved in data analysis and statistics; Renata M.
Perez contributed to concept, design, data analysis,
interpretation, statistics, and critical revision of the
article; Jose ´ Osmar Medina Pestana was involved in
data collection and critical revision of the article;
Vale ´ ria Pereira Lanzoni was involved in histologi-
cal analysis and critical revision of the article; Ivon-
ete Sandra Souza e Silva contributed to data
analysis and critical revision of the article; Antonio
Eduardo Benedito Silva contributed to data analy-
sis, interpretation, and critical revision of the arti-
cle; and Maria Lucia Cardoso Gomes Ferraz was
involved in concept, design, data analysis, interpre-
tation, statistics, and critical revision of the article.
1. FABRIZI F, LUNGHI G, GANESHAN SV, MARTIN P, MESSA P.
Hepatitis C virus infection and the dialysis patient. Semin
Dial 2007: 20: 416.
2. FABRIZI F, MARTIN P, DIXIT V, BUNNAPRADIST S, DULAI G.
Hepatitis C virus antibody status and survival after renal
transplantation: meta-analysis of observational studies.
Am J Transplant 2005: 5: 1452.
3. RAHNAVARDI M, HOSSEINI MOGHADDAM SM, ALAVIAN SM.
Hepatitis C in hemodialysis patients: current global magni-
tude, natural history, diagnostic difficulties, and preventive
measures. Am J Nephrol 2008: 28: 628.
4. RAO KV, ANDERSON WR, KASISKE BL, DAHL DC. Value of
liver biopsy in the evaluation and management of chronic
liver disease in renal transplant recipients. Am J Med
1993: 94: 241.
5. MATHURIN P, MOUQUET C, POYNARD T et al. Impact of
hepatitis B and C virus on kidney transplantation out-
come. Hepatology 1999: 29: 257.
6. ROCHA CM, PEREZ RM, FERREIRA AP et al. Efficacy and
tolerance of interferon-alpha in the treatment of chronic
hepatitis C in end-stage renal disease patients on hemodial-
ysis. Liver Int 2006: 26: 305.
7. GLICKLICH D, THUNG SN, KAPOIAN T, TELLIS V, REINUS
JF. Comparison of clinical features and liver histology in
hepatitis C-positive dialysis patients and renal transplant
recipients. Am J Gastroenterol 1999: 94: 159.
8. ROTH D, ZUCKER K, CIROCCO R et al. A prospective study
of hepatitis C virus infection in renal allograft recipients.
Transplantation 1996: 61: 886.
9. ALRIC L, DI-MARTINO V, SELVES J et al. Long-term impact
of renal transplantation on liver fibrosis during hepatitis C
virus infection. Gastroenterology 2002: 123: 1494.
10. PEREZ RM, FERREIRA AS, MEDINA-PESTANA JO et al. Is
hepatitis C more aggressive in renal transplant patients
than in patients with end-stage renal disease? J Clin
Gastroenterol 2006: 40: 444.
11. LUDWIG J. The nomenclature of chronic active hepatitis:
an obituary. Gastroenterology 1993: 105: 274.
12. DESMET VJ, GERBER M, HOOFNAGLE JH, MANNS M, SCHE-
UER PJ. Classification of chronic hepatitis: diagnosis, grad-
ing and staging. Hepatology 1994: 19: 1513.
13. GURSOY M, BILEZIKCI B, COLAK T et al. Histologic out-
come of hepatitis C virus infection in renal transplant
recipients and the effect of pretransplantation interferon
treatment. Transplant Proc 2000: 32: 558.
14. HURAIB S, IQBAL A, TANIMU D, ABDULLAH A. Sustained
virological and histological response with pretransplant
interferon therapy in renal transplant patients with chronic
viral hepatitis C. Am J Nephrol 2001: 21: 435.
15. OLSON MR, GREWAL KS, BINGAMAN A et al. An interna-
tional survey of the diagnosis, management, and treatment
of hepatitis C in patients with end-stage renal disease. Exp
Clin Transplant 2009: 7: 203.
16. LOCATELLI F, DEL VECCHIO L, MANZONI C. Morbidity and
mortality on maintenance haemodialysis. Nephron 1998:
17. BUARGUB MA. 5-year mortality in hemodialysis patients: a
single center study in Tripoli. Saudi J Kidney Dis Transpl
2008: 19: 268.
Uehara et al.
18. DEMIRHAN B, BOYACIOGLU S, KART H, TELATAR H. Histo- Download full-text
pathological features of hepatitis C virus infection in
patients with chronic renal failure and renal transplanta-
tion. Transplant Proc 1996: 28: 2328.
19. HANAFUSA T, ICHIKAWA Y, KISHIKAWA H et al. Retrospec-
tive study on the impact of hepatitis C virus infection on
kidney transplant patients over 20 years. Transplantation
1998: 66: 471.
20. LEGENDRE C, GARRIGUE V, LE BIHAN C et al. Harmful
long-term impact of hepatitis C virus infection in kidney
transplant recipients. Transplantation 1998: 65: 667.
21. PEREIRA BJ, LEVEY AS. Hepatitis C infection in cadaver
organ donors: strategies to reduce transmission of infec-
tion and prevent organ waste. Pediatr Nephrol 1995: 9
22. CAILLARD S, LELONG C, PESSIONE F, MOULIN B. Post-trans-
plant lymphoproliferative disorders occurring after renal
transplantation in adults: report of 230 cases from the
French Registry. Am J Transplant 2006: 6: 2735.
23. SABHARWAL S, DELGADO-BORREGO A, CHUNG RT. Extrahe-
patic hepatitis C virus after transplantation: diabetes and
renal dysfunction. Liver Transpl 2008: 14(Suppl 2): S51.
24. FABRIZI F, LUNGHI G, FINAZZI S et al. Decreased serum
aminotransferase activity in patients with chronic renal
failure: impact on the detection of viral hepatitis. Am J
Kidney Dis 2001: 38: 1009.
25. NATOV SN, PEREIRA BJ. Management of hepatitis C infec-
tion in renal transplant recipients. Am J Transplant 2002:
Hepatitis C: evolution post-renal transplantation