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• W2006161692 abstract "The prevention, diagnosis, and treatment of hepatitis C Virus (HCV) infection are clearly important for the management of patients undergoing chronic hemodialysis, because (i) the HCV infection rate is high in dialysis patients; (ii) the outcome is poorer in HCV-infected than non-infected dialysis patients; and (iii) an improvement in the outcome can be expected by the prevention or diagnosis and treatment of HCV infection. Therefore, it was decided to prepare “guidelines for the treatment and management of hepatitis C at dialysis facilities by dialysis physicians and nephrologists in cooperation with hepatologists” by the instruction of Tadao Akizawa, Chairman of the Board of Directors of the Japanese Society for Dialysis Therapy, and Hideki Hirakata, Chairman of the Scientific Committee, and under the leadership of Tadashi Tomo, Chairman of the Committee for the Preparation of the Guidelines. In preparing the guidelines, it was agreed (i) that they would be applied to chronic dialysis patients; and (ii) that they would be used by physicians at dialysis facilities. They would also be prepared to inform hepatologists about the dose of interferon and the criteria for the introduction and reduction of interferon administration in dialysis patients. Their preparation was initiated at the first meeting of the Committee for the Preparation of Guidelines for the Treatment of Hepatitis C Virus Infection in Dialysis Patients on 6 January 2009. Prior to this, in April 2008, the Kidney Disease: Improving Global Outcomes (KDIGO) group presented the “KDIGO Clinical Practice Guidelines for the Prevention, Diagnosis, Evaluation, and Treatment of Hepatitis C in Chronic Kidney Disease” as the first guidelines by the KDIGO itself in Kidney International1. The guidelines were a 107-page tour de force consisting of five chapters dealing with (i) detection and evaluation of HCV in CKD patients; (ii) treatment of HCV-infected CKD patients; (iii) prevention of HCV infection in the dialysis room; (iv) treatment of HCV infected patients before and after kidney transplantation; and (v) diagnosis and treatment of HCV-related retinopathy, were compiled under the supervision of Michel Jadoul and David Roth, and described the diagnosis, treatment, and prevention of HCV infection in patients with CKD in the maintenance period, dialysis patients, and patients undergoing kidney transplantation. The ISN informed its members of these guidelines and recommended to apply them in consideration of the state of each country, region, and facility (implantation), because they contained provisions not necessarily based on strong evidence. Thus, the Working Group for the Preparation of the Guidelines for the Treatment of Hepatitis C Virus Infection decided to make the guidelines cover the (i) diagnosis, (ii) treatment, and (iii) prevention of HCV infection in dialysis patients, and (iv) their management before and after transplantation on the basis of the items of the KDIGO guidelines by securing the cooperation of experts in dialysis and HCV hepatitis. In addition, as the aminotransferase levels are low in dialysis patients, and as the method for the assessment of fibrosis was not established, some members considered it necessary to include test methods and diagnostic criteria, and the guidelines were decided to comprise five chapters dealing with (i) screening, (ii) management (methods and frequencies of blood tests and imaging studies), (iii) indications of antiviral therapies, (iv) treatment by antiviral therapies (including patients expected to receive kidney transplantation), and (v) prevention of HCV infection at hemodialysis facilities. The references consisted primarily of English and Japanese literature published by the end of 2008, but domestic and overseas guidelines were also included. All members listed above have submitted a conflict of interest disclosure report to the General Affairs Committee. The evidence and recommendation levels were prepared on the basis of the position paper “Grading evidence and recommendations for clinical practice guidelines in nephrology”2 issued by KDIGO in 2006 and the Working Group Report on the Grading of Evidence Levels and Degrees of Recommendation disclosed by the Japanese Society for Dialysis Therapy on 16 November 2009 (Table 1) (later published in the Journal of the Japanese Society for Dialysis Therapy with modifications) 3. The serum aminotransferase levels are lower in dialysis patients than in individuals with normal renal function. (Evidence level: High, Recommendation level: Strong) The serum aminotransferase levels are higher in HCV-antibody-positive than in negative dialysis patients, but the criteria for the general population cannot be applied to dialysis patients. (Evidence level: High, Recommendation level: Strong) In dialysis patients, it is desirable to measure the serum aminotransferase levels at least once a month even if they are asymptomatic. (Evidence level: Low, Recommendation level: Weak) It is recommended to perform the HCV antibody test and, if necessary, the HCV-RNA test at the introduction of dialysis and the acceptance of patients. (Evidence level: Low, Recommendation level: Strong) In dialysis patients, it is desirable to perform the HCV antibody test at least once every 6 months even if HCV antibody is negative on the initial test. (Evidence level: Low, Recommendation level: Weak) If the serum aminotransferase level increases with no clear cause, it is recommended to perform an ad hoc HCV-RNA or HCV core antigen test in addition to the HCV antibody test. (Evidence level: Low, Recommendation level: Strong) If an HCV-positive patient considered to be due to nosocomial infection that has been detected, it is recommended to perform the HCV-RNA or HCV core antigen test in all dialysis patients who may have been exposed. (Evidence level: Very low, Recommendation level: Strong) Serum aminotransferase levels (AST, ALT) as indices of liver function have been reported to be lower in dialysis patients than in individuals with normal kidney function. There has been a report that the ALT level was 15.6 ± 12 IU/L in dialysis patients and 22.7 ± 18 IU/L in normal controls and that the upper limit of the normal range of ALT in dialysis patients was 27 IU/mL 1. Thus, if the upper limit of the normal range was set at 25 IU/L, then the ALT level was normal in 67% of dialysis patients 2. There is also a report that the AST levels in healthy individuals and dialysis patients were 22.3 (22.0 ± 22.7) and 20.6 (21.6 ± 23.6), respectively, that the ALT levels were 20.3 (19.9 ± 20.7) and 16.3 (15.3 ± 17.3), respectively, and that the cutoff values effective for the prediction of HCV infection were 18 for AST and 16 for ALT 3. Since the serum aminotransferase levels are lower in dialysis patients than the standards in the general population, their cutoff values for the prediction of HCV infection should be set at lower levels in these patients. It has been known that the serum aminotransferase levels in uremic patients are low and negatively correlate with the blood urea nitrogen level 4, and factors that inhibit the serum aminotransferase activities have been reported to accumulate in patients’ serum with elevations of the serum aminotransferase levels due to dialysis 5. However, the level of pyridoxal-5’-phosphate (PLP) is positively correlated with the AST and ALT levels. Additionally, serum aminotransferase levels were significantly lower in the PLP-deficient group than in the normal group, being 9.2 ± 0.3 vs. 13.4 ± 0.7 for AST and 8.6 ± 0.6 vs. 11.4 ± 0.9 for ALT. Also, as the AST and ALT levels were elevated by supplementation of PLP only in the PLP-deficient group, deficiency of PLP, which acts as a coenzyme of aminotransferases, has been suggested to partly explain the low aminotransferase levels in dialysis patients 6. There is also a report that, in uremia, the enzyme activity of PLP is lost as its lysine-binding site is carbamylated by cyanogen salts formed by urea 7. In contrast, it has also been reported that the Vitamin B6 and PLP levels are normal in dialysis patients and thus, the low serum aminotransferase levels cannot be explained by Vitamin B6 deficiency 8, 9. Therefore, based on the clinical observations to date and abnormalities of enzyme activities in uremic patients, serum aminotransferase levels are considered to be lower in dialysis patients than in people with normal kidney function. The serum aminotransferase levels are normal in dialysis patients regardless of whether they are negative or positive for HCV antibody. However, the ALT level is higher in HCV antibody positive dialysis patients than in HCV antibody negative dialysis patients (2.7 ± 20.0 and 12.5 ± 8.8, respectively) 10. Particularly, the simultaneous detection of HB antigen and HCV-RNA has been related to ALT elevation. Also, it has been reported that the ALT level was 32.4 ± 24.2 and 33.7 ± 27.2 in male and female HCV-antibody-positive dialysis patients, respectively, but 17.0 ± 11.4 and 13.9 ± 6.1 in male and female HCV-antibody-negative patients, respectively. The ALT level was also reported to be higher in HCV-RNA-positive than in HCV RNA negative patients. However, the ALT level was not related to the HCV genotype 11. In HCV-antibody-positive, HCV-antibody-negative, HCV-RNA-positive, and HCV-antibody-negative dialysis patients, the ratio of ALT/upper limit of the normal range was 0.77 ± 0.57, 0.38 ± 0.23, 0.81 ± 0.57, and 0.37 ± 0.23, respectively. The cutoff value of ALT for being HCV-antibody-positive as determined from the receiver operating characteristic (ROC) curve was 50% of the upper limit of the normal range (sensitivity: 67%, specificity: 83%) and that for being HCV-RNA-positive was 45% (sensitivity: 71%, specificity 80%). Also, the observed value/upper limit of normal range of ALT was clearly higher in HCV-RNA-positive than in HCV-RNA-negative dialysis patients 12. Moreover, this value was reported not to differ in the group without hepatitis but to be higher in the group with hepatitis compared with the group without hepatitis, suggesting that the ALT level of HCV-RNA-positive dialysis patients may be useful as a marker of liver disorder obtained by liver biopsy 13. However, histological findings obtained by liver biopsy were reported to be milder, and the ALT level to be lower, in HCV-positive dialysis patients than in HCV-positive individuals with normal kidney function 14, 15. Therefore, the serum aminotransferase levels are considered to be higher in HCV-antibody-positive dialysis patients than in those negative, but the criteria for the general population are not considered to be applicable to dialysis patients. While there is no evidence concerning the frequency of measurement of the serum aminotransferase levels in dialysis patients, there have been reports that the serum aminotransferase levels and the ratio of ALT/upper limit of the normal range has been reported to be higher in HCV-antibody-positive and HCV-RNA-positive patients than in negative patients 10-12, 16. Although the ALT level was elevated in only 51% of the HCV-RNA-positive patients after kidney transplantation, but that the ALT level was correlated with the degree of liver tissue damage evaluated by liver biopsy, and that ALT can serve as a marker of liver tissue damage in HCV-RNA-positive recipients of kidney transplantation 13. Therefore, observation of changes in ALT levels by regular examinations may lead to the early detection of HCV infection, and the possibility of HCV infection must always be considered even if the serum aminotransferase levels are within the normal ranges. Liver function tests are usually performed once a month in dialysis patients. It is desirable to measure the serum aminotransferase levels at least once a month even in asymptomatic patients. In HCV-positive chronic nephritis, there has been a report that membranoproliferative glomerulonephritis was the most frequent, accounting for 54%, that cryoglobulinemia was noted in 54% of the patients, and that HCV-RNA was detected in 66% on cryoprecipitation and 22% of frozen sections 17. Immunocomplexes are noted in the glomeruli by kidney biopsy, and they have been shown to be a cause of chronic nephritis such as membranoproliferative glomerulonephritis in which factors such as cryoglobulin are involved 18-21. The HCV antibody-positive rate is 7.9% in patients with kidney diseases compared with 1.03% in healthy individuals and is particularly high (16.6%) in patients with glomerulonephritis. This rate is higher in those patients with a Ccr level of less than 30 mL/min than in patients with a Ccr level of 30 mL/min or higher (13% vs. 2.7%). Furthermore, HCV infection has been reported to be involved in the etiology of glomerulonephritis 22. There has also been a report that HCV was positive in 3.9% of the 1041 CKD patients, and that 95% of HCV-positive patients showed viremia, and that the HCV-positive rate is high in CKD patients 23. It has also been reported that HCV antibody was positive in 12.7% of dialysis patients, and that of the dialysis patients, the HCV-antibody-positive rate was higher in those with non-insulin dependent diabetes mellitus (NIDDM) (20.8%) than in those with no diabetes mellitus (DM) (10%) 24, and that the HCV-positive rate in NIDDM patients was high at 19.5% 25. Based on these reports, HCV infection is likely to be involved in the pathogenesis of chronic kidney diseases. Therefore, the HCV-antibody-positive rate has been reported to be high at 7.3% 26 or 14.4% 27 in dialysis patients at the introduction of dialysis therapy. Moreover, according to the Dialysis Outcomes and Practice Patterns Study (DOPPS), the HCV-positive rate varied from 2.6% to 22.9% among the participating countries, and its increases were related to the dialysis period, male gender, black race, diabetes status, HBV infection, kidney transplantation, and alcohol and drug dependence. Many other studies have clarified the wide differences in the HCV-antibody-positive rate and the HCV-antibody-positive-conversion rate among dialysis patients at different facilities 28, 29. Particularly, the HCV-positive-conversion rate has been reported to be high at facilities with a high HCV-positive rate 30. Therefore, it is recommended to perform HCV antibody or HCV-RNA test at the introduction of dialysis therapy or at transfer of patients to another hospital. While there is no evidence concerning the frequency of HCV antibody test in dialysis patients, HCV positivity was reported to be detected in 70 days (36–210 days) by second-generation enzyme immunoassay (EIA) and in 49 days (27–119 days) by the third generation EIA from the detection of abnormality of ALT. In patients with acute HCV hepatitis, HCV-RNA becomes detectable in 1–2 weeks after HCV infection, and chronic HCV hepatitis is diagnosed when HCV-RNA persists for 6 months or longer. The chronicity rate is 55–85%. In acute HCV hepatitis cases, the ALT level begins to increase 2–8 weeks after infection. Symptoms usually appear 3–12 weeks (mean 7 weeks) after infection, and HCV antibody become positive simultaneously or with a slight delay. If the infection takes a chronic course, the ALT level increases and changes. Some immune-deficient individuals remain HCV-antibody-negative even after HCV infection 31. In a previous study, the HCV-RNA-positive-rate increased from 12.9% to 15.7% after a 4-year follow-up, de novo HCV infection was observed in one patient during this period with an HCV-positive-conversion rate of 0.33%/year, and the initial examination is considered to have been made during the window period in five of the patients, so that it was concluded that the HCV-RNA test must be performed once a month to reduce nosocomial HCV infection 32. Also, there is a report that the HCV-antibody positive conversion rate was 0.44%/year when examined at 6-month intervals while observing the CDC standard preventive measures 33. Therefore, the KDIGO guidelines recommend to perform the HCV antibody test in HCV-antibody-negative patients once every 6–12 months (intermediate recommendation level) 34. The KDIGO also recommends testing by the enzyme antibody method at facilities with a low HCV infection rate and by the nucleic acid amplification technique at those with a high HCV infection rate (intermediate recommendation level) 34. Based on these observations, it is considered desirable to perform the HCV antibody test at least once every 6 months in dialysis patients even if the HCV antibody were negative on the initial test. If the serum aminotransferase level has increased with no obvious reason, there is the possibility of HCV infection. It has been reported that 9% of dialysis patients were HCV-RNA-positive even if they were HCV-antibody-negative, and the viral level is considered to have been low in such patients. Caution is needed in immune-deficient individuals such as dialysis patients because of a low viral level 35. Therefore, HCV infection cannot be excluded on the basis of a negative HCV antibody test, the HCV-RNA test must be performed when considered necessary. For the HCV-RNA assay, real-time PCR is recommended because of its high sensitivity 36, 37. It has also been reported that patients become positive for the HCV core antigen 2 days after HCV infection but do not become positive for the HCV antibody until 50.8 days after infection. Thus a high-sensitivity assay for the HCV core antigen that is an inexpensive and quick method for the judgment of HCV infection, is useful for the diagnosis of HCV infection and is used during the window period until HCV antibody becomes positive 38, 39. KDIGO recommends that the HCV test by a nucleic acid amplification technique should be carried out if the serum aminotransferase level has increased with no clear reason (strong recommendation) 34. Also, the determination of the viral level and HCV genotype by the HCV-RNA assay contributes to the evaluation of responses to interferon therapy 36. Thus if the serum aminotransferase level has increased with no clear cause, it is recommended to perform the HCV-RNA or HCV core antigen test ad hoc in addition to the HCV antibody test. If a patient is judged to be newly positive on the HCV antibody test, the possibility of a nosocomial outbreak of HCV infection must be examined. As mentioned in the comment for Statement 6, the possibility of HCV infection cannot be excluded in patients who may have been exposed even if they are HCV-antibody-negative. Also, to fill the window period of HCV infection, a test for HCV-RNA or HCV core antigen must be performed. KDIGO recommends that surveillance to examine whether nosocomial infection has not occurred by the HCV-RNA test using a nucleic acid amplification technique be carried out if an HCV-positive patient considered to be due to nosocomial infection has been detected (strong recommendation). In addition, KDIGO recommends re-examination within 2–12 weeks after an initial negative examination (weak recommendation) 34. Therefore, if an HCV-positive patient considered to be due to nosocomial infection has been detected, it is recommended to carry out the HCV-RNA or HCV core antigen test in all dialysis patients who may have been exposed. Similar to patients with normal renal function, liver biopsy is the most reliable method to evaluate the liver disease of HCV-infected dialysis patients. It is mostly recommended, when transplantation is considered. (Evidence level: Low, Recommendation level: Weak) The prognosis is significantly worse in HCV-infected dialysis patients than in uninfected dialysis patients. (Evidence level: High, Recommendation level: None) It is recommended to periodically follow-up HCV-infected dialysis patients to screen for liver cirrhosis and early detection of hepatocellular carcinoma. (Evidence level: High, Recommendation level: Strong) Iron has hepatocyte toxicity, and excessive hepatic iron deposition is an exacerbating factor of chronic hepatitis C and promotes hepatocarcinogenesis. In consideration of these facts, it is desirable to avoid iron overload in HCV-infected dialysis patients. (Evidence level: Low, Recommendation level: Weak) Similar to HCV-infected patients with normal renal function, liver biopsy is the most reliable method to evaluate the liver disease in HCV-infected dialysis patients. It is mostly recommended when kidney transplantation is considered. (Evidence level: Low, Recommendation level: Weak) In dialysis patients, the aminotransferase levels are often low even when they are infected with HCV, and liver biopsy is the most reliable method to evaluate the liver disease of HCV-infected dialysis patients as well as HCV-infected patients with normal renal function. Concerning histological changes of the liver, there have been many reports that inflammation and fibrosis are observed less frequently in HCV-infected dialysis patients than in HCV-infected patients with normal renal function 1-5. Cotler et al. 3 showed that HCV-infected dialysis patients had less inflammatory activity and a lower proportion of bridging fibrosis or cirrhosis than in hepatitis C patients with normal renal function. In addition, as a histological finding by liver biopsy, Shiavon et al. 4 and Hu et al. 6 reported that HCV-infected dialysis patients showed stage III and IV severe fibrosis significantly less frequently than those with normal renal function. Also, Sterling et al. 7 noted that the severity of liver fibrosis and liver cirrhosis was similar to that in hepatitis C patients with normal renal function showing a normal ALT level but was milder than in those showing a high ALT level. There is also a report that the progression rate of liver fibrosis corrected for the infected period was relatively slow 8. However, de Paula Farah et al. 9 have reported that histological findings of both fibrosis and inflammation are comparable between HCV-infected dialysis patients and HCV-infected patients with normal renal function. On histological examination of the liver in HCV-infected dialysis patients before kidney transplantation, severe liver fibrosis or cirrhosis was noted in 5.5–32%, and liver cirrhosis was noted in 0–24% 2, 3, 5-8, 10, 11. The survival rate of dialysis patients with biopsy-proven cirrhosis during 10 years after transplantation was low at 26%, indicating that liver cirrhosis is an independent risk factor of poor prognosis, and liver cirrhosis is a contraindication for kidney transplantation 12. It has also been clarified that the prevalence of liver disorders after transplantation increases markedly (five times) if there is HCV infection before transplantation 13, and that the progression of hepatic lesions is faster in HCV-infected kidney transplantation patients than in HCV-infected patients with normal kidney function 14. Since the results of blood tests are not correlated with these histological changes of the liver, it is necessary to evaluate histological changes by liver biopsy before kidney transplantation 5, 7, 10, 11, 15, 16. In dialysis patients, it has been reported that percutaneous liver biopsy can be performed safely 17, but it generally increases the risk of hemorrhage. Transjugular liver biopsy is safer but is not performed widely. The prognosis is significantly worse in HCV-infected dialysis patients than in uninfected dialysis patients. (Evidence level: High, Recommendation level: None) In 90% or more of dialysis patients, HCV infection leads to chronic hepatitis 18. The effects of HCV infection on the prognosis of dialysis patients have become an important issue due to the increase in patients with longer dialysis duration. Many studies have indicated that the prognosis of HCV-infected dialysis patients is significantly worse than that of uninfected dialysis patients 19-25. According to meta-analysis by Fabrizi et al. 26, adjusted relative risk of all-cause mortality in HCV-infected dialysis patients was 1.34 on the basis of seven clinical studies involving 11 589 patients. Causes of death related to liver diseases such as hepatocellular carcinoma and liver cirrhosis were 5.89 times more frequent in the former group. The incidence of liver cirrhosis in HCV-infected dialysis patients varies among reports from 1.3–12.5% 10, 11, 16, 27. According to the investigation by Akiba et al. 28, the incidence of liver cirrhosis in HCV-antibody-positive dialysis patients was 8.57/1000/year. There have been a few reports that the prognosis of liver disease is better in HCV-infected dialysis patients than in patients with normal renal function. Okuda et al. 29 reported that none of the 189 patients with HCV-infected dialysis patients showed progression to liver cirrhosis. Also, Ishida et al. 30 showed by a questionnaire survey of 6366 dialysis patients that hepatocellular carcinoma and liver cirrhosis were observed in 1.8% and 8.6%, respectively, which were lower than the percentages in patients with normal renal function. However, reports regarding the progression of liver diseases have been inconsistent, with an 8-year prospective cohort study by Espinosa et al. 31 showing the rapid progression to liver cirrhosis in dialysis patients, being observed after a median of 7 years from the initial elevation in ALT, which is in contrast to the general population. Generally, the incidence of hepatocellular carcinoma in HCV-infected patients is proportionate to the severity of liver fibrosis, and its incidence in patients with liver cirrhosis showing severest fibrosis is reported to be about 8%/year 32. However, there is no detailed report on the incidence of hepatocellular carcinoma in HCV-infected dialysis patients. Nakayama et al. 20 followed up 276 HCV-antibody-positive dialysis patients over 6 years and reported liver cirrhosis in 30 and hepatocellular carcinoma in eight at the end of the follow-up period. If most hepatocellular carcinomas are assumed to have occurred in liver cirrhosis, the annual rate of progression from liver cirrhosis to hepatocellular carcinoma is considered to be at least 4%. The finding that liver cirrhosis was noted in 30 (13.2%) of the 276 patients suggests that the progression rate to liver cirrhosis is nearly the same as that in non-dialysis patients. In dialysis patients, the incidence of, and mortality due to, cancers have often been reported to be higher than in the general population. According to a report from Italy, the incidence of hepatocellular carcinoma is 2.41 times higher in dialysis patients than in those with normal renal function 33. According to a study in Okinawa, Japan, the incidence of cancer in dialysis patients was 2.48 times higher in males and 3.99 times higher in females than that in the general population, but the incidence of hepatocellular carcinoma was similar in males and lower in females compared with that in the general population 34. In a prospective study of a cohort of 233 HCV-infected dialysis patients, hepatocellular carcinoma was observed in three patients during 10 years (0.53%/year) 35. According to a questionnaire survey of 67 970 patients, the incidence of hepatocellular carcinoma was reported to be 3.87/1000 HCV-infected dialysis patients/year during a 3-year period 28. At the end of 1999, the prevalence of liver cirrhosis was 8.25% and 11.84% in HCV-antibody-positive patients and HCV-RNA-positive dialysis patients, respectively, and that of hepatocellular carcinoma was 2.16% and 2.59%, respectively. In those coinfected with HBV and HCV, the prevalences of liver cirrhosis and hepatocellular carcinoma were 12.2% and 2.7%, respectively 36. In patients coinfected with HBV and HCV, liver damage is notable even in those with normal renal function. However, as the same is observed also in HCV-infected dialysis patients 8, particularly close follow-up is needed. To date, there has been no control study comparing the prognosis between HCV-infected dialysis patients and HCV-infected patients with normal renal function. This comparison may be difficult because of the reduced life expectancy in dialysis patients. There has been no report on the prognosis-improving effect of therapeutic intervention in HCV-infected dialysis patients. Reports on the viral load level in dialysis patients have been inconsistent: It has been reported to be low by some 37, 38, not to differ by others 2, 39, and to be high in still others 6. The HCV RNA levels were reported to decrease in dialysis patients but not to change in the control group during a 3-year follow-up by Furusyo et al. 38 and during a 10-year follow-up by Okuda et al. 29, respectively. In a comparison concerning comobidities, hypertension, hepatitis B, liver cirrhosis, wasting, anemia, and HIV infection were more prevalent, but coronary artery disease and stroke were less prevalent in 5737 HCV-infected dialysis patients than in 11 228 uninfected dialysis patients matched for the time at which dialysis was initiated. On the other hand, there is also a report that coronary artery disease was more prevalent in HCV-infected dialysis patients 40. It is recommended to periodically follow-up HCV-infected dialysis patients for the diagnosis of liver cirrhosis and early detection of hepatocellular carcinoma. (Evidence level: High, Recommendation level: Strong) HCV-infected dialysis patients develop liver cirrhosis or hepatocellular carcinoma more frequently than uninfected dialysis patients, and periodic follow-up for the diagnosis of liver cirrhosis and early detection of hepatocellular carcinoma is necessary. Follow up testing to evaluate the progression of liver disease (liver fibrosis, liver cirrhosis, hepatocellular carcinoma) include blood tests of AST, ALT, γ-GTP, total bilirubin, albumin, platelet count, and AST/platelet ratio and imaging techniques such as abdominal ultrasonography and contrast-enhanced CT. Since the AST and ALT levels are low in d" @default.
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• W2006161692 date "2012-06-11" @default.
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• W2006161692 title "2011 Japanese Society for Dialysis Therapy Guidelines for the Treatment of Hepatitis C Virus Infection in Dialysis Patients" @default.
• W2006161692 cites W1552014912 @default.
• W2006161692 cites W158937586 @default.
• W2006161692 cites W1874253413 @default.
• W2006161692 cites W1942247157 @default.
• W2006161692 cites W1968706953 @default.
• W2006161692 cites W1970448649 @default.
• W2006161692 cites W1975523149 @default.
• W2006161692 cites W1975765367 @default.
• W2006161692 cites W1976385423 @default.
• W2006161692 cites W1977253900 @default.
• W2006161692 cites W1977484015 @default.
• W2006161692 cites W1977897254 @default.
• W2006161692 cites W1979446275 @default.
• W2006161692 cites W1980421411 @default.
• W2006161692 cites W1981830762 @default.
• W2006161692 cites W1985808254 @default.
• W2006161692 cites W1991062024 @default.
• W2006161692 cites W1991815197 @default.
• W2006161692 cites W1993818972 @default.
• W2006161692 cites W1993960896 @default.
• W2006161692 cites W1994213343 @default.
• W2006161692 cites W1994694609 @default.
• W2006161692 cites W1995300274 @default.
• W2006161692 cites W1995491828 @default.
• W2006161692 cites W1998855827 @default.
• W2006161692 cites W2001919720 @default.
• W2006161692 cites W2002492308 @default.
• W2006161692 cites W2003369651 @default.
• W2006161692 cites W2005190929 @default.
• W2006161692 cites W2007961349 @default.
• W2006161692 cites W2008480868 @default.
• W2006161692 cites W2009590546 @default.
• W2006161692 cites W2010234430 @default.
• W2006161692 cites W2011053501 @default.
• W2006161692 cites W2012985982 @default.
• W2006161692 cites W2013740507 @default.
• W2006161692 cites W2015042366 @default.
• W2006161692 cites W2015336471 @default.
• W2006161692 cites W2015509647 @default.
• W2006161692 cites W2015689674 @default.
• W2006161692 cites W2018117762 @default.
• W2006161692 cites W2018548370 @default.
• W2006161692 cites W2018782141 @default.
• W2006161692 cites W2018953484 @default.
• W2006161692 cites W2019356022 @default.
• W2006161692 cites W2020614899 @default.
• W2006161692 cites W2022561069 @default.
• W2006161692 cites W2023418418 @default.
• W2006161692 cites W2027203857 @default.
• W2006161692 cites W2028177473 @default.
• W2006161692 cites W2028684272 @default.
• W2006161692 cites W2029663482 @default.
• W2006161692 cites W2035239781 @default.
• W2006161692 cites W2044633884 @default.
• W2006161692 cites W2046339229 @default.
• W2006161692 cites W2047208492 @default.
• W2006161692 cites W2048163738 @default.
• W2006161692 cites W2049904028 @default.
• W2006161692 cites W2050109801 @default.
• W2006161692 cites W2050949661 @default.
• W2006161692 cites W2052801481 @default.
• W2006161692 cites W2055058760 @default.
• W2006161692 cites W2056179599 @default.
• W2006161692 cites W2060229598 @default.
• W2006161692 cites W2061733249 @default.
• W2006161692 cites W2065803035 @default.
• W2006161692 cites W2065996764 @default.
• W2006161692 cites W2066989725 @default.
• W2006161692 cites W2072712324 @default.
• W2006161692 cites W2073592039 @default.
• W2006161692 cites W2074274907 @default.
• W2006161692 cites W2080311291 @default.
• W2006161692 cites W2080416536 @default.
• W2006161692 cites W2082154943 @default.
• W2006161692 cites W2084908925 @default.
• W2006161692 cites W2085967046 @default.
• W2006161692 cites W2086595268 @default.
• W2006161692 cites W2086620101 @default.
• W2006161692 cites W2087073512 @default.
• W2006161692 cites W2087493145 @default.
• W2006161692 cites W2088053309 @default.

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