The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform
Chun Sang Li - One of the best experts on this subject based on the ideXlab platform.
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spontaneous renal allograft rupture attributed to Acute Tubular Necrosis
American Journal of Kidney Diseases, 1999Co-Authors: Yiu Han Chan, Kim Ming Wong, Chun Sang LiAbstract:Abstract A renal allograft recipient receiving triple immunosuppressive therapy developed spontaneous allograft rupture 5 days after her second cadaveric renal transplantation. Renal biopsy showed interstitial edema with severe Acute Tubular Necrosis (ATN). There was no evidence of Acute rejection or renal vein thrombosis. The ruptured renal graft was salvaged by an aggressive fluid resuscitation therapy and surgical hemostasis. The renal function was satisfactory on discharge. We conclude that renal allograft rupture can be the result of interstitial edema solely attributed to ATN in the absence of graft rejection. The ruptured graft kidney is potentially salvageable for those patients whose hemodynamic status can be stabilized by appropriate supportive therapy.
Yiu Han Chan - One of the best experts on this subject based on the ideXlab platform.
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spontaneous renal allograft rupture attributed to Acute Tubular Necrosis
American Journal of Kidney Diseases, 1999Co-Authors: Yiu Han Chan, Kim Ming Wong, Chun Sang LiAbstract:Abstract A renal allograft recipient receiving triple immunosuppressive therapy developed spontaneous allograft rupture 5 days after her second cadaveric renal transplantation. Renal biopsy showed interstitial edema with severe Acute Tubular Necrosis (ATN). There was no evidence of Acute rejection or renal vein thrombosis. The ruptured renal graft was salvaged by an aggressive fluid resuscitation therapy and surgical hemostasis. The renal function was satisfactory on discharge. We conclude that renal allograft rupture can be the result of interstitial edema solely attributed to ATN in the absence of graft rejection. The ruptured graft kidney is potentially salvageable for those patients whose hemodynamic status can be stabilized by appropriate supportive therapy.
Kim Ming Wong - One of the best experts on this subject based on the ideXlab platform.
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spontaneous renal allograft rupture attributed to Acute Tubular Necrosis
American Journal of Kidney Diseases, 1999Co-Authors: Yiu Han Chan, Kim Ming Wong, Chun Sang LiAbstract:Abstract A renal allograft recipient receiving triple immunosuppressive therapy developed spontaneous allograft rupture 5 days after her second cadaveric renal transplantation. Renal biopsy showed interstitial edema with severe Acute Tubular Necrosis (ATN). There was no evidence of Acute rejection or renal vein thrombosis. The ruptured renal graft was salvaged by an aggressive fluid resuscitation therapy and surgical hemostasis. The renal function was satisfactory on discharge. We conclude that renal allograft rupture can be the result of interstitial edema solely attributed to ATN in the absence of graft rejection. The ruptured graft kidney is potentially salvageable for those patients whose hemodynamic status can be stabilized by appropriate supportive therapy.
Jianghua Chen - One of the best experts on this subject based on the ideXlab platform.
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BMEI - Prediction of renal transplant rejection and Acute Tubular Necrosis in renal transplant based on SVM
2012 5th International Conference on BioMedical Engineering and Informatics, 2012Co-Authors: Xun Li, Yao Wang, Chengxuan Wang, Sanqing Hu, Ying Xu, Jianghua ChenAbstract:Prevention and proper treatment of renal transplant rejection and Acute Tubular Necrosis in kidney are the key to improving the long-term kidney transplant survival rate. Hence, it is important to predict the Acute renal graft rejection in early stage. In recent years, there emerged some biomarkers measured through non-invasive techniques that may indicate the Acute rejection. In this paper, we apply SVM method to analyze biomarkers, medullary R2* (MR2*) and cortical R2* (CR2*) in transplanted kidney, acquired through BOLD MRI for classification of patients with normally functioning kidney transplants and Acute rejection in kidney, including Acute allograft rejection and Acute Tubular Necrosis. Furthermore, we use the classification model to predict the Acute kidney rejection. The results show that the application of SVM in the analysis of CR2* and MR2* has its potential in prediction of Acute rejection in kidney.
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Prediction of renal transplant rejection and Acute Tubular Necrosis in renal transplant based on SVM
2012 5th International Conference on BioMedical Engineering and Informatics, 2012Co-Authors: Xun Li, Yao Wang, Chengxuan Wang, Sanqing Hu, Ying Xu, Jianghua ChenAbstract:Prevention and proper treatment of renal transplant rejection and Acute Tubular Necrosis in kidney are the key to improving the long-term kidney transplant survival rate. Hence, it is important to predict the Acute renal graft rejection in early stage. In recent years, there emerged some biomarkers measured through non-invasive techniques that may indicate the Acute rejection. In this paper, we apply SVM method to analyze biomarkers, medullary R2* (MR2*) and cortical R2* (CR2*) in transplanted kidney, acquired through BOLD MRI for classification of patients with normally functioning kidney transplants and Acute rejection in kidney, including Acute allograft rejection and Acute Tubular Necrosis. Furthermore, we use the classification model to predict the Acute kidney rejection. The results show that the application of SVM in the analysis of CR2* and MR2* has its potential in prediction of Acute rejection in kidney.
Wenjuan Wang - One of the best experts on this subject based on the ideXlab platform.
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proliferative capacity of stem progenitor like cells in the kidney may associate with the outcome of patients with Acute Tubular Necrosis
Human Pathology, 2011Co-Authors: Youxin Ye, Bingyin Wang, Xinxin Jiang, Weiming Hu, Jian Feng, Hua Li, Yingjuan Ying, Wenjuan WangAbstract:Summary Animal studies indicate that adult renal stem/progenitor cells can undergo rapid proliferation in response to renal injury, but whether the same is true in humans is largely unknown. To examine the profile of renal stem/progenitor cells responsible for Acute Tubular Necrosis in human kidney, double and triple immunostaining was performed using proliferative marker and stem/progenitor protein markers on sections from 10 kidneys with Acute Tubular Necrosis and 4 normal adult kidneys. The immunopositive cells were recorded using 2-photon confocal laser scanning microscopy. We found that dividing cells were present in the tubules of the cortex and medulla, as well as the glomerulus in normal human kidney. Proliferative cells in the parietal layer of Bowman capsule expressed CD133, and dividing cells in the tubules expressed immature cell protein markers paired box gene 2, vimentin, and nestin. After Acute Tubular Necrosis, Ki67-positive cells in the cortex tubules significantly increased compared with normal adult kidney. These Ki67-positive cells expressed CD133 and paired box gene 2, but not the cell death marker, activated caspase-3. In addition, the number of dividing cells increased significantly in patients with Acute Tubular Necrosis who subsequently recovered, compared with patients with Acute Tubular Necrosis who consequently developed protracted Acute Tubular Necrosis or died. Our data suggest that renal stem/progenitor cells may reside not only in the parietal layer of Bowman capsule but also in the cortex and medulla in normal human kidney, and the proliferative capacity of renal stem/progenitor cells after Acute Tubular Necrosis may be an important determinant of a patient's outcome.
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Proliferative capacity of stem/progenitor-like cells in the kidney may associate with the outcome of patients with Acute Tubular Necrosis.
Human Pathology, 2011Co-Authors: Youxin Ye, Bingyin Wang, Xinxin Jiang, Weiming Hu, Jian Feng, Hua Li, Yingjuan Ying, Wenjuan WangAbstract:Summary Animal studies indicate that adult renal stem/progenitor cells can undergo rapid proliferation in response to renal injury, but whether the same is true in humans is largely unknown. To examine the profile of renal stem/progenitor cells responsible for Acute Tubular Necrosis in human kidney, double and triple immunostaining was performed using proliferative marker and stem/progenitor protein markers on sections from 10 kidneys with Acute Tubular Necrosis and 4 normal adult kidneys. The immunopositive cells were recorded using 2-photon confocal laser scanning microscopy. We found that dividing cells were present in the tubules of the cortex and medulla, as well as the glomerulus in normal human kidney. Proliferative cells in the parietal layer of Bowman capsule expressed CD133, and dividing cells in the tubules expressed immature cell protein markers paired box gene 2, vimentin, and nestin. After Acute Tubular Necrosis, Ki67-positive cells in the cortex tubules significantly increased compared with normal adult kidney. These Ki67-positive cells expressed CD133 and paired box gene 2, but not the cell death marker, activated caspase-3. In addition, the number of dividing cells increased significantly in patients with Acute Tubular Necrosis who subsequently recovered, compared with patients with Acute Tubular Necrosis who consequently developed protracted Acute Tubular Necrosis or died. Our data suggest that renal stem/progenitor cells may reside not only in the parietal layer of Bowman capsule but also in the cortex and medulla in normal human kidney, and the proliferative capacity of renal stem/progenitor cells after Acute Tubular Necrosis may be an important determinant of a patient's outcome.
