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1.
BMC Nephrol ; 19(1): 254, 2018 10 05.
Article in English | MEDLINE | ID: mdl-30290778

ABSTRACT

BACKGROUND: ABO-incompatible living related kidney transplantation (ABO-iLKT) has increased the possibilities for kidney transplantation in patients with end stage renal disease. Due to advancements in immunosuppressive agents and the identification of immunological conditions following ABO-iLKT, this transplantation technique has achieved the same success rate as ABO-compatible LKT. However, some patients continue to generate anti-blood type antibodies, despite conventional immunosuppressant treatment. CASE PRESENTATION: A 60-year-old man was referred to our hospital for kidney transplantation. The proposed transplant was ABO incompatible, from a donor with blood-type A to a recipient with blood-type O. The recipient's anti-A blood-type IgG antibody titer was measured at 4096-fold dilution. Following desensitization therapy, including mycophenolate mofetil (MMF) 750 mg/day for 3 months, intravenous Rituximab 200 mg, and two sessions of double filtration plasmapheresis, the anti-A blood-type IgG antibody titer decreased to only 516-fold dilution and did not meet our target of less than 128-fold dilution. MMF was thus continued for an additional 4 months and four additional sessions of plasmapheresis were undertaken. Following these interventions, antibody titers decreased to 128-fold dilution and ABO-iLKT was performed. Following transplant, antibody-mediated rejection was not observed and renal function was preserved. However, a post-operative renal biopsy 1.5 months later showed evidence of T-cell-mediated rejection IB. The patient was treated with steroids, with no increase in serum creatinine. CONCLUSION: Our findings suggest that the long-term single MMF desensitization therapy could be a suitable option for ABO-iLKT with high refractory and rebound anti-blood type antibody. Further studies are required to establish the optimal immunosuppression regimen to control B cell- mediated immunity in ABO-iLKT.


Subject(s)
ABO Blood-Group System/immunology , Blood Group Incompatibility , Desensitization, Immunologic , Immunoglobulin G/blood , Immunosuppressive Agents/therapeutic use , Kidney Transplantation/methods , Living Donors , Mycophenolic Acid/therapeutic use , Humans , Kidney Failure, Chronic/surgery , Male , Middle Aged , Plasmapheresis , Rituximab/therapeutic use
2.
Oncotarget ; 8(13): 20881-20894, 2017 Mar 28.
Article in English | MEDLINE | ID: mdl-28152509

ABSTRACT

Previous studies showed that five miRNAs (miR-885-5p, miR-1274, miR-210-3p, miR-224 and miR-1290) were upregulated the most in clear cell renal cell carcinoma (ccRCC). Our focus was to understand from a clinical standpoint the functional consequences of upregulating miR-210-3p. Towards this, we utilized the CRISPR/Cas9 gene editing system to deplete miR-210-3p in RCC cell lines (786-o, A498 and Caki2) and characterized the outcomes. We observed that miR-210-3p depletion dramatically increased tumorigenesis, including altering the morphology of A498 and Caki2 cells in a manner characteristic of epithelial-mesenchymal transition (EMT). These results were corroborated by in vivo xenograft studies, which showed enhanced growth of tumors from miR-210-3p-depleted A498 cells. We identified Twist-related protein 1 (TWIST1) as a key target of miR-210-3p. Analysis of the ccRCC patient data in The Cancer Genome Atlas database showed a negative correlation between miR-210-3p and TWIST1 expression. High TWIST1 and low miR-210-3p expression associated with poorer overall and disease-free survival as compared to low TWIST1 and high miR-210-3p expression. These findings suggest that renal cell carcinoma progression is promoted by TWIST1 suppression mediated by miR-210-3p.


Subject(s)
CRISPR-Cas Systems/genetics , Carcinoma, Renal Cell/pathology , Cell Transformation, Neoplastic/pathology , Gene Expression Regulation, Neoplastic , Kidney Neoplasms/pathology , MicroRNAs/antagonists & inhibitors , Nuclear Proteins/metabolism , Twist-Related Protein 1/metabolism , Animals , Apoptosis , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Carcinoma, Renal Cell/genetics , Carcinoma, Renal Cell/metabolism , Cell Movement , Cell Proliferation , Cell Transformation, Neoplastic/genetics , Cell Transformation, Neoplastic/metabolism , Epithelial-Mesenchymal Transition , Female , Humans , Kidney Neoplasms/genetics , Kidney Neoplasms/metabolism , Mice , Mice, Inbred BALB C , Mice, Nude , MicroRNAs/genetics , Neoplasm Staging , Nuclear Proteins/genetics , Prognosis , Survival Rate , Tumor Cells, Cultured , Twist-Related Protein 1/genetics , Xenograft Model Antitumor Assays
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