The Experts below are selected from a list of 4017 Experts worldwide ranked by ideXlab platform
Ahmed Halawa - One of the best experts on this subject based on the ideXlab platform.
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A case of high drain output after Renal transplantation: Review of current evidence
Archives of Organ Transplantation - Peertechz Publications, 2018Co-Authors: Sajid Mohmad, Ajay Sharma, Ahmed HalawaAbstract:Surgical complications are not uncommon after Renal transplantation. They should always be in the differential diagnosis of Renal Graft Dysfunction. While ruling out or confirming a surgical cause of Graft Dysfunction, a sequential approach should be undertaken starting from clinical examination and moving on to more invasive investigations as the clinical picture becomes clearer. Biochemical assay of drain fluid is important. Causes of a collection around/near the Graft include abscess, hematoma, urinoma and lymphocele. Treatment of each of them is different. Causes of urinoma can be donor derived or surgical technique related. SPECT/CT may be needed to confirm the location of urinary leak. Treatment of the urinoma depends on its severity and location. Small and distal lesions can be treated conservatively while as larger and proximal leaks need surgical intervention. Ureteric stenting may be undertaken as a prophylaxis against urinary leak.Lymphoceles should always be considered as a cause of perinephric collection in Renal transplant. It can be differentiated from a urinoma by the concentration of creatinine in the drain fluid. The treatment may be conservative or surgical depending on the size of the lymphocele and initial response or resistance to conservative management. Scenario: A 28-year-old CKD 5 underwent a kidney transplantation from his brother with primary function. Post-surgery, the drain is quite productive (820 mls on day 2 and 750 mls on day 3). Drain fluid biochemistry showed K of 28 mmol/L and creatinine of 16000 μmol/l. His serum creatinine on that day was 416 μmol/l and serum K is 5.1 mmol/L.
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a case of high drain output after Renal transplantation review of current evidence
Archives of Organ Transplantation, 2018Co-Authors: Sajid Mohmad, Ajay Sharma, Ahmed HalawaAbstract:Surgical complications are not uncommon after Renal transplantation. They should always be in the differential diagnosis of Renal Graft Dysfunction. While ruling out or confirming a surgical cause of Graft Dysfunction, a sequential approach should be undertaken starting from clinical examination and moving on to more invasive investigations as the clinical picture becomes clearer. Biochemical assay of drain fluid is important. Causes of a collection around/near the Graft include abscess, hematoma, urinoma and lymphocele. Treatment of each of them is different.
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the early diagnosis of acute Renal Graft Dysfunction a challenge we face the role of novel biomarkers
Annals of Transplantation, 2011Co-Authors: Ahmed HalawaAbstract:Acute Graft Dysfunction can be caused by ischaemic damage or immunological injury leading to serious consequences both in the short and long term. We are in a desperate need for biomarkers of immune and nonimmune injury at different time points of the transplantation time course, beginning from a potential kidney donors where acute kidney damage can pass unnoticed, during the early post-transplant periods to predict acute transplant Dysfunction due to various causes and during long term follow up to predict chronic histological changes. The implementation of these novel biomarkers could increase the sensitivity of diagnosis and monitoring of kidney injury in kidney transplant recipients. Traditionally acute Graft Dysfunction is diagnosed by measuring serum creatinine concentrations. Unfortunately rise in serum creatinine is a late sign of kidney damage. It indicates rather predicts the damage. The treatment, in order to be effective, must be instituted very early after the initiating insult, well before the serum creatinine even begins to rise. Fortunately, emerging technologies such as functional genomics and proteomics have uncovered novel candidates that are emerging as potentially useful biomarkers of acute kidney injury (AKI). The most promising of biomarkers in AKI for clinical use include a plasma panel consisting of Neutrophil Gelatinase-Associated Lipocalin (NGAL) and Cystatin C and a urine panel including NGAL, Il-18 and Kidney Injury Molecule 1 (KIM-1). Most of these biomarkers were developed in non-transplant AKI, yet their role in clinical transplantation has to be identified.
Haiwei Yang - One of the best experts on this subject based on the ideXlab platform.
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impaired atg16l dependent autophagy promotes Renal interstitial fibrosis in chronic Renal Graft Dysfunction through inducing endmt by nf κb signal pathway
Frontiers in Immunology, 2021Co-Authors: Zeping Gui, Chuanjian Suo, Zijie Wang, Ming Zheng, Shuang Fei, Hao Chen, Li Sun, Zhijian Han, Jun Tao, Haiwei YangAbstract:Chronic Renal Graft Dysfunction (CAD) is caused by multiple factors, including glomerular sclerosis, inflammation, interstitial fibrosis and tubular atrophy (IF/TA). However, the most prominent elements of CAD are IF/TA. Our studies have confirmed that endothelial-mesenchymal transition (EndMT) is an important source to alloGraft IF/TA. The characteristic of EndMT is the loss of endothelial marker and the acquisition of mesenchymal or fibroblastic phenotypes. Autophagy is an intracellular degradation pathway that is regulated by autophagy-related proteins and plays a vital role in many fibrotic conditions. However, whether or not autophagy contributes to fibrosis of Renal alloGraft and how such mechanism occurs still remains unclear. Autophagy related 16 like gene (ATG16L) is a critical autophagy-related gene (ARG) necessary for autophagosome formation. Here, we first analyzed kidney transplant patient tissues from Gene Expression Omnibus (GEO) datasets and 60 transplant patients from our center. Recipients with stable kidney function were defined as non-CAD group and all patients in CAD group were histopathologically diagnosed with CAD. Results showed that ATG16L, as one significant differential ARG, was less expressed in CAD group compared to the non-CAD group. Furthermore, we found there were less autophagosomes and autolysosomes in transplanted kidneys of CAD patients, and downregulation of autophagy is a poor prognostic factor. In vitro, we found out that the knockdown of ATG16L enhanced the process of EndMT in human Renal glomerular endothelial cells (HRGECs). In vivo, the changes of EndMT and autophagic flux were then detected in rat Renal transplant models of CAD. We demonstrated the occurrence of EndMT, and indicated that abundance of ATG16L was accompanied by the dynamic autophagic flux change along different stages of kidney transplantation. Mechanistically, knockdown of ATG16L, specifically in endothelial cells, reduced of NF-κB degradation and excreted inflammatory cytokines (IL-1β, IL-6 and TNF-α), which could facilitate EndMT. In conclusion, ATG16L-dependent autophagic flux causing by transplant showed progressive loss increase over time. Inflammatory cytokines from this process promoted EndMT, thereby leading to progression of CAD. ATG16L served as a negative regulator of EndMT and development of Renal Graft fibrosis, and autophagy can be explored as a potential therapeutic target for chronic Renal Graft Dysfunction.
Herwig-ulf Meier-kriesche - One of the best experts on this subject based on the ideXlab platform.
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Value of posttransplant antibody tests in the evaluation of patients with Renal Graft Dysfunction.
American Journal of Transplantation, 2007Co-Authors: Juan C. Scornik, Giselle Guerra, Jesse D. Schold, Titte R. Srinivas, Duska Dragun, Herwig-ulf Meier-kriescheAbstract:Posttransplant HLA antibodies correlate with C4d positive rejection and decreased Graft survival. However, the diagnostic value of various antibody tests in the management of patients presenting with Graft Dysfunction is uncertain. Whether all or some patients should be tested, how often, what antibodies to test for and how to interpret results in presensitized or transfused patients, are issues still unresolved. We tested for HLA and non-HLA antibodies by flow cytometry assays in 103 consecutive patients with Graft Dysfunction. The results show that: (1) C4d positive rejection was diagnosed in 75% of patients who developed posttransplant HLA antibodies, but only in 2% in antibody negative patients. (2) The correlation existed for donor specific IgG antibodies but not for IgM or nondonor specific IgG antibodies. (3) Weak antibody reactivity required confirmation by alternative testing as there were false positive results. (4) Posttransplant transfusions did not induce de novo HLA antibodies. (5) Negative antibody results were unlikely to turn positive after several months of follow-up. (6) Antibodies to the angiotensin II type 1 receptor, HLA-DP and MICA did not correlate with C4d+ rejection. We conclude that testing for posttransplant HLA antibodies is critical in narrowing the diagnostic alternatives in patients with Graft Dysfunction.
Magali Giral - One of the best experts on this subject based on the ideXlab platform.
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baff and baff r levels are associated with risk of long term kidney Graft Dysfunction and development of donor specific antibodies
American Journal of Transplantation, 2012Co-Authors: A Thibaultespitia, Yohann Foucher, Richard Danger, T Migone, Annaick Pallier, Stephanie Castagnet, C Ggueguen, A Devys, A Cgautier, Magali GiralAbstract:There are lines of evidence that B cells may play a role in transplantation. B cell activating factor, BAFF, is a homotrimer that has been shown to play a role in B cell survival, maturation and activation. To date, little is known of the role of BAFF and its receptors in transplantation. We analyzed the level of BAFF mRNA and its soluble protein, as well as transcripts coding for its receptors, BAFF-R, TACI and BCMA, in the blood of 143 patients with stable kidney transplant function 5 years or more posttransplantation. Three endpoints were analyzed: the time to Renal Dysfunction, the time to appearance of anti-HLA antibodies and the time to development of donor-specific antibodies. We established threshold values for BAFF and BAFF-R and showed that (1) stable patients with high BAFF-R levels had a higher risk of developing Graft Dysfunction, (2) patients with lower levels of BAFF transcripts or a higher level of soluble BAFF had a significantly higher risk of developing donor-specific antibodies. These data suggest that BAFF constitutes a risk factor for Renal Graft Dysfunction and development of donor-specific antibodies. They also suggest that agents targeting BAFF-R interactions may offer new therapeutic opportunities in transplantation.
Zeping Gui - One of the best experts on this subject based on the ideXlab platform.
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impaired atg16l dependent autophagy promotes Renal interstitial fibrosis in chronic Renal Graft Dysfunction through inducing endmt by nf κb signal pathway
Frontiers in Immunology, 2021Co-Authors: Zeping Gui, Chuanjian Suo, Zijie Wang, Ming Zheng, Shuang Fei, Hao Chen, Li Sun, Zhijian Han, Jun Tao, Haiwei YangAbstract:Chronic Renal Graft Dysfunction (CAD) is caused by multiple factors, including glomerular sclerosis, inflammation, interstitial fibrosis and tubular atrophy (IF/TA). However, the most prominent elements of CAD are IF/TA. Our studies have confirmed that endothelial-mesenchymal transition (EndMT) is an important source to alloGraft IF/TA. The characteristic of EndMT is the loss of endothelial marker and the acquisition of mesenchymal or fibroblastic phenotypes. Autophagy is an intracellular degradation pathway that is regulated by autophagy-related proteins and plays a vital role in many fibrotic conditions. However, whether or not autophagy contributes to fibrosis of Renal alloGraft and how such mechanism occurs still remains unclear. Autophagy related 16 like gene (ATG16L) is a critical autophagy-related gene (ARG) necessary for autophagosome formation. Here, we first analyzed kidney transplant patient tissues from Gene Expression Omnibus (GEO) datasets and 60 transplant patients from our center. Recipients with stable kidney function were defined as non-CAD group and all patients in CAD group were histopathologically diagnosed with CAD. Results showed that ATG16L, as one significant differential ARG, was less expressed in CAD group compared to the non-CAD group. Furthermore, we found there were less autophagosomes and autolysosomes in transplanted kidneys of CAD patients, and downregulation of autophagy is a poor prognostic factor. In vitro, we found out that the knockdown of ATG16L enhanced the process of EndMT in human Renal glomerular endothelial cells (HRGECs). In vivo, the changes of EndMT and autophagic flux were then detected in rat Renal transplant models of CAD. We demonstrated the occurrence of EndMT, and indicated that abundance of ATG16L was accompanied by the dynamic autophagic flux change along different stages of kidney transplantation. Mechanistically, knockdown of ATG16L, specifically in endothelial cells, reduced of NF-κB degradation and excreted inflammatory cytokines (IL-1β, IL-6 and TNF-α), which could facilitate EndMT. In conclusion, ATG16L-dependent autophagic flux causing by transplant showed progressive loss increase over time. Inflammatory cytokines from this process promoted EndMT, thereby leading to progression of CAD. ATG16L served as a negative regulator of EndMT and development of Renal Graft fibrosis, and autophagy can be explored as a potential therapeutic target for chronic Renal Graft Dysfunction.