الفهرس 
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Abstract
Liver disease is one of the leading causes of death in long-term survivors
after kidney transplantation. Chronic liver disease is a frequent complication
affecting about 15 % of renal allograft recipients. Infection by hepatitis B and C
viruses is the predominant cause of hepatic dysfunction in these patients.
Hepatic cirrhosis and clinically active hepatitis due to HBV and HCV infection
clearly contraindicate kidney transplantation. More controversial is the attitude
to be adopted towards candidates with clinically quiescent chronic HBV or
HCV. It was proved by many authors that schistosomiasis does not affect short
as well as long-term outcome of kidney transplantation.
In an attempt to study the impact of pretransplant liver dysfunction and
etiology of liver disease on the short-term outcome of renal transplantation, we
prospectively followed up 75-end stage renal disease patients on regular
hemodialysis and arranged for living donor kidney transplantation at Mansoura
Urology and Nephrology Center from the pre- to post-transplant period.
The patients were classified into two main groups:
Group (1): twenty-five patients with healthy liver considered a control group
Group (2): fifty patients with abnormal liver function of different etiologies.
So, they were subclassified into:
Subgroup (a): patients with HCV antibodies and I or HCV RNA positive
(28 patients); (i) Treated by interferon (before transplantation): 16 patients
and (ii) Non-treated by interferon: 12 patients
Subgroup (b): patients with mixed HCV and HBV infection (5 patients).
Subgroup (d: patients with mixed HCV and schistosoma! infection (8
patients).
Subgroup (d): patients with Schistosomiasis (9 patients)
We noticed high sustained response to IFN in HCV viremic haemodialysis
patients (68.2 %) which is much better than non-uremic HCV positive patients
and only one patient turned HCV RNA positive after renal transplantation. Also,
we found that HCV patients treated by IFN as well as pure schistosomal renal
allograft recipients had excellent graft function during the period of follow up
and significantly better than other groups. Moreover, number of rejection
episodes was nearly equal to the control group.
Also, we found that HCV (not treated by lFN) showed non-significant
elevation of serum creatinine especially during the first 8 months after kidney
transplantation. However, after that, serum creatinine DROPped and was nonsignificantly
different from the control group.
The mixed HCV and HBV infection group showed significant pretransplant
impaired liver function in comparison to control group. After kidney
transplantation, serum creatinine was non-significantly higher than control
group especially during the first year after transplantation. Moreover, the
number of rejection episodes was non-significantly higher than control group.
Unfortunately, mixed HCV and schistosomiasis group had bad results.
Only 2S % did not experience rejection, 2S % experienced 2 episodes and 50 %
experienced more than 3 rejection episodes during their follow up period. Their
serum creatinine ranged from 1-12 mg / dl (mean 2.S mg / dl) versus 0.6-3.4 mg
/ dl (mean 1.24 mg /dl) in control group. Also, their serum creatinine reached its
peak in the 7th month (4.94 versus 1.5 mg /dl). Moreover, number of rejection
episodes was nearly double that of control group (2.38 versus 1.24) but it was
non-significant due to high standard deviation.
None of our patients developed fulminant hepatitis or chronic liver
disease.
In summary, our presented data confirmed that IFN is highly effective in
management of pretransplant HCV infection which may contribute to better
post-transplant graft function. Neighther HCV nor schistosomiasis affect the
short term out come either of the patients or of the graft survival after kidney
transplantation. Mixed HCV and HBV may cause more susceptibility to early
post-transplant graft impairment and more rejection episodes. Also, mixed HCY
and schistosomiasis was associated with post-transplant graft impairment. So, it
carries a high risk to patients as well as graft survival after kidney
transplantation.
We conclude that problems occurring in renal transplant recipients must be
diagnosed as early as possible to avoid either irreversible rejection or a rapidly
fatal outcome: the management of these patients appears to be one of the most
important factors for the long term success of an allograft. Such management
must be performed by a well-trained clinical and laboratory consultants. One
must keep in mind that an otherwise benign disease can be rapidly lethal in a
transplant recipient
Again, we conclude that pre-transplant treatment of HCY in chronic renal
failure patients by interferon is highly effective in management of pretransplant
HCY infection which may contribute to better post-transplant graft function.
Also, patients with mixed HCY and Schistosomal infection are liable to bad
post-transplant results either in the patient or the graft survival.
We recommend IFN therapy for HCY RNA positive haemodialysis
patients and caution must be taken in renal transplantation to patients with
mixed HCY and Schistosomiasis. Further studies are needed to complete this
work, to detect the possible pathogenesis of impaired graft survival in mixed
HCY and schistosomiasis patients and postulation of new regimens of
immunosuppression therapy suitable to these patients as well as close
monitoring of graft function after kidney transplantation.