Due to the early nosocomial spread of HCV within hemodialysis
units (Fabrizi 2007), the infection is highly prevalent in this
setting and the treatment of CHC in this population remains a
challenge to clinicians.
A meta-analysis on the impact of HCV infection on mortality in
the dialysis population (seven observational studies enrolling
11,589 subjects on maintenance hemodialysis) showed a
detrimental impact of HCV on survival in patients with chronic
kidney disease (Fabrizi 2008). Positive anti-HCV serological
status after kidney transplantation is implicated in the
pathogenesis of acute glomerulopathy, “de novo” graftassociated
nephropathy, new-onset diabetes mellitus, and
increased incidence of infections.
There are good data to support antiviral therapy in the
pretransplant patients (see chapter 5). The decision to treat such
a difficult subgroup of patients should be based on liver
histology, age, comorbidities, and ability to tolerate therapy. In a
meta-analysis of patients on maintenance hemodialysis, the
overall SVR was 37% in the whole group and 30% in patients with
HCV genotype 1 (Fabrizi 2008). The viral response to
monotherapy with standard interferon in maintenance
hemodialysis patients is higher than that observed in patients
with CHC and normal kidney function (7-16%), due to the
following factors: lower VL, milder histological forms of liver
injury, a decreased interferon clearance, and an increase in
endogenous interferon release from circulating white blood cells
during hemodialysis procedures.
Data on PegIFN monotherapy and PegIFN/RBV therapy in
hemodialysed patients are limited. Very low amounts of RBV are
removed via dialysis, leading to drug accumulation and
exacerbating hemolysis in this population, already at significant
risk for anemia. Therefore, the decision to use combination
therapy in hemodialysed patients should take into consideration
several precautions: 1) use of very low RBV doses
units (Fabrizi 2007), the infection is highly prevalent in this
setting and the treatment of CHC in this population remains a
challenge to clinicians.
A meta-analysis on the impact of HCV infection on mortality in
the dialysis population (seven observational studies enrolling
11,589 subjects on maintenance hemodialysis) showed a
detrimental impact of HCV on survival in patients with chronic
kidney disease (Fabrizi 2008). Positive anti-HCV serological
status after kidney transplantation is implicated in the
pathogenesis of acute glomerulopathy, “de novo” graftassociated
nephropathy, new-onset diabetes mellitus, and
increased incidence of infections.
There are good data to support antiviral therapy in the
pretransplant patients (see chapter 5). The decision to treat such
a difficult subgroup of patients should be based on liver
histology, age, comorbidities, and ability to tolerate therapy. In a
meta-analysis of patients on maintenance hemodialysis, the
overall SVR was 37% in the whole group and 30% in patients with
HCV genotype 1 (Fabrizi 2008). The viral response to
monotherapy with standard interferon in maintenance
hemodialysis patients is higher than that observed in patients
with CHC and normal kidney function (7-16%), due to the
following factors: lower VL, milder histological forms of liver
injury, a decreased interferon clearance, and an increase in
endogenous interferon release from circulating white blood cells
during hemodialysis procedures.
Data on PegIFN monotherapy and PegIFN/RBV therapy in
hemodialysed patients are limited. Very low amounts of RBV are
removed via dialysis, leading to drug accumulation and
exacerbating hemolysis in this population, already at significant
risk for anemia. Therefore, the decision to use combination
therapy in hemodialysed patients should take into consideration
several precautions: 1) use of very low RBV doses
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