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RISS 인기검색어
- 검색키워드
- 저자 : ( Marina Khvan ) (검색결과 2 건)
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( Marina Khvan ),( Nazym Nigmatullina ),( Saltanat Rakhimzhanova ),( Samat Issakov ),( Venera Altynova ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Introduction: Hepatitis C virus (HCV) infection is an important co-morbidity in patients after kidney transplantation (KT) affecting patient and graft survival. In the era of Direct Acting Antiviral (DAA) drugs the current standards of management strongly suggest to treat HCV positive patient with end-stage renal disease (ESRD) before KT. However, in the conditions where this treatment is not available, KT remains the only lifesaving option for children with ESRD who is not able to sustain on dialysis any longer. Aim: Currently, there is limited data available about outcomes of pediatric patients with HCV after kidney transplantation. We studied the prevalence, clinical profile and outcome of HCV infection in KT pediatric recipients (KTPR) in Kazakhstan for the first time after the launching the National Pediatric KT Program in 2012. Methods: We studied pediatric patients who underwent KT from January 2012 to December 2018 at the Department of Nephrology, Dialysis and Transplantation, National Research Center of Mother and Child Health, University Medical Center, Nur-Sultan. HCV infection was defined as a positive anti-HCV antibody and/or HCV RNA PCR positivity. Control group included KTPRs with no evidence of HCV or hepatitis B virus (HBV) infection. Results: A total of 73 KTPRs were included. The mean age was 10.6 ± 4.5 years, male:female ratio was 1:1 and mean duration of post-transplant follow-up was 32 months. 9 patients (12%) had evidence of HCV infection. All HCV-positive patients underwent KT before DAAs were available in the country. Among them 4 patients were treated with interferon before KT, 4 patients had HCV infection by the time of KT and 1 patient developed de-novo HCV infection after KT. Although there was no statistical significant difference in patient survival (logrank P=0.82) and graft survival (log-rank P=0.416) between HCV-positive group and controls, the only death in HCV group was registered in the patient who had de-novo HCV infection after KT. 2 patients who were treated from HCV infection before KT lost their kidney grafts and returned on dialysis. Among 4 patients with persistent HCV infection by the time of KT, 2 were successfully treated with DAAs 5 years after KT without any side effects or worsening of graft function. 2 KTPRs still have chronic HCV infection Stage 0 - 1 with low viral load, normal liver function tests and normal kidney graft function over the 6 years after KT. Conclusions: In our cohort HCV-positive KTPRs did not have any difference in patient and graft survival comparing to KTPRs without HCV infection. The worst outcome had patient with de-novo developed HCV infection after KT. HCV treatment with DAA after KT was successful without deterioration of kidney graft function. Limitation: low number of HCV-positive KTPRs.
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An, Gun Hee,Yun, Jintak,Hong, Yu Ah,Khvan, Marina,Chung, Byung Ha,Choi, Bum Soon,Park, Cheol Whee,Choi, Yeong Jin,Kim, Yong-Soo,Yang, Chul Woo Hindawi Publishing Corporation 2014 Journal of immunology research Vol.2014 No.-
<P>The treatment for chronic active antibody-mediated rejection (CAMR) remains controversial. We investigated the efficacy of rituximab (RTX) and intravenous immunoglobulin (IVIg) for CAMR. Eighteen patients with CAMR were treated with RTX (375 mg/m<SUP>2</SUP>) and IVIg (0.4 g/kg) for 4 days. The efficacy of RTX/IVIg combination therapy (RIT) was assessed by decline in estimated glomerular filtration rate per month (ΔeGFR) before and after RIT. Patients were divided into responder and nonresponder groups based on decrease and no decrease in ΔeGFR, respectively, and their clinical and histological characteristics were compared. Response rate to RIT was 66.7% (12/18), and overall ΔeGFR decreased significantly to 0.4 ± 1.7 mL<I>·</I>min<SUP>−1</SUP><I>·</I>1.73 m<SUP>−2</SUP> per month 6 months after RIT compared to that observed 6 months before RIT (1.8 ± 1.0, <I>P</I> < 0.05). Clinical and histological features between the 12 responders and the 6 nonresponders were not significantly different, but nonresponders had a significantly higher proteinuria levels at the time of RIT (2.5 ± 2.5 versus 7.0 ± 3.5 protein/creatinine (g/g), <I>P</I> < 0.001). The effect of the RIT on ΔeGFR had dissipated in all patients by 1 year post-RIT. Thus, RIT delayed CAMR progression, and baseline proteinuria level was a prognostic factor for response to RIT.</P>
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