Transplanted Kidney (transplanted + kidney)

Distribution by Scientific Domains


Selected Abstracts


Pediatrics Access Problems in hemodialysis with a permanent central venous catheter

HEMODIALYSIS INTERNATIONAL, Issue 1 2005
J. Muscheites
Hemodialysis is a common treatment of chronic renal failure, also in childhood. Due to the high standard of technique there are only few contraindications for this treatment at present. Limitations are given by the vessel access. But in the last years, hemodialysis has been made practicable by the permanent central venous catheter, however, with more problems. As an example for potential complications in the treatment with the permanent catheter we present an unusual case report about a twenty-one- year-old girl suffering from chronic renal failure due to reflux nephropathy, Prader-Willi- syndrome, myelonatrophia of undetermined origin with spastic diplegia of the legs, and increasing sphincter ani dysfunction. We started the renal replacement therapy when the girl was 15 years old. It was not possible to create an AV fistula due to very small vessels. Two Gore-Tex ® implants were clotted in absence of thrombophilia. Afterwards, the hemodialysis was performed by a permanent central venous catheter. The catheter had to be changed 15 times. The reasons for changing the catheter were problems of flow during hemodialysis due to clotting, dislocations, spontaneous removing of the catheter by herself, and infections. Altogether a sepsis occurred four times. The first transplantation failed due to a rupture of the transplanted kidney. A second transplantation was not possible because of the high BMI. Intermittently, the girl was treated with peritoneal dialysis (PD) in the hospital, because the PD couldn't be done at home due to different reasons. Only on weekends could the girl go home. The PD had to be finished after 6 months due to a severe psychotic syndrome. The girl died at age 21, caused by a sepsis following the 15th change of the catheter. A huge problem of frequent catheter changing is the limited availability of vessel accesses , the limits of treatment by hemodialysis. [source]


Medication adherence patterns in adult renal transplant recipients,

RESEARCH IN NURSING & HEALTH, Issue 6 2006
Cynthia L. Russell
Abstract Patient adherence to immunosuppressive medications adherence is crucial to survival of the patient and a transplanted kidney, yet adherence is variable. Using a prospective, descriptive design, immunosuppressive medication adherence of 44 renal transplant recipients was followed for 6 months at a Midwestern transplant center using electronic monitoring. Four medication adherence patterns emerged from a hierarchical cluster analysis: those who took medications on time, those who took medications on time with late/missed doses, those who rarely took medications on time and who were late with morning and/or evening doses, and those who missed doses. This study is a step toward developing and implementing interventions targeted to specific patterns of poor adherence. © 2006 Wiley Periodicals, Inc. Res Nurs Health 29: 521,532, 2006 [source]


Donor and Recipient Origin of Mesenchymal and Endothelial Cells in Chronic Renal Allograft Remodeling

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 3 2009
H. Rienstra
Chronic transplant dysfunction (CTD) is the leading cause for limited kidney graft survival. Renal CTD is characterized by interstitial and vascular remodeling leading to interstitial fibrosis, tubular atrophy and transplant vasculopathy (TV). The origin of cells and pathogenesis of interstitial and vascular remodeling are still unknown. To study graft-versus-recipient origin of interstitial myofibroblasts, vascular smooth muscle cells (SMCs) and endothelial cells (ECs), we here describe a new rat model for renal CTD using Dark Agouti kidney donors and R26 human placental alkaline phosphatase transgenic Fischer344 recipients. This model showed the development of CTD within 12 weeks after transplantation. In interstitial remodeling, both graft- and recipient-derived cells contributed to a similar extent to the accumulation of myofibroblasts. In arteries with TV, we observed graft origin of neointimal SMCs and ECs, whereas in peritubular and glomerular capillaries, we detected recipient EC chimerism. These data indicate that, within the interstitial and vascular compartments of the transplanted kidney, myofibroblasts, SMCs and ECs involved in chronic remodeling are derived from different sources and suggest distinct pathogenetic mechanisms within the renal compartments. [source]


Aortic aneurysm repair with a functioning renal transplant: therapeutic options

ANZ JOURNAL OF SURGERY, Issue 1-2 2004
Denise M. Roach
Background: Aortic aneurysm repair in the presence of a functioning renal transplant carries significant risks of renal ischaemia. We describe the management of patients undergoing this treatment by using a temporary, externally sited axillofemoral bypass and discuss other treatment options. Methods: Three patients underwent a temporary, externally sited axillary artery to common femoral artery bypass. The aneurysm was then dissected via a transperitoneal incision. When the aneurysm was clamped, the axillofemoral graft was opened allowing retrograde perfusion to the renal transplant. Results: All three patients made a good recovery without postoperative deterioration of renal function. Conclusion: Numerous methods of protecting the transplanted kidney have been described, including expeditious surgery with no renal protection or some form of temporary shunt to perfuse the donor iliac artery. Temporary insertion of an axillofemoral bypass adds 45,60 min of extra operating time if two surgeons are present. However, this technique should completely avoid transplant ischaemia and is an excellent technique for dealing with abdominal aneurysms in patients with functioning transplants. [source]


Generalized lymphedema in a sirolimus-treated renal transplant patient

CLINICAL TRANSPLANTATION, Issue 2 2008
Carmine De Bartolomeis
Abstract:, Generalized lymphedema is an extremely rare effect of sirolimus therapy in renal transplant recipients. We describe the development of this complication in a 56-yr-old woman, who was given an experimental protocol with cyclosporine, sirolimus, steroids, and basiliximab. Following the protocol, after one month, the patient was randomized to the "sirolimus only" group, while cyclosporine was completely suspended and the oral steroids were continued. Three months later, the patient was admitted for severe lymphedema of the lower limbs, with significant weight increase, massive ascites and dyspnea, but excellent renal function. A chest radiography and an ultrasound study of the heart showed a moderate pleural and pericardial effusion. An abdominal ultrasound scan showed two small lymphoceles next to the transplanted kidney, confirmed with a CT scan. After sirolimus discontinuation the generalized lymphedema started to improve and three months later all the symptoms had disappeared. [source]


Peritubular capillary C4d deposition and renal outcome in post-transplant IgA nephropathy

CLINICAL TRANSPLANTATION, Issue 2 2007
Jung Choi
Abstract:, Backgrounds:, Immunological staining of the transplanted kidney for C4d in peritubular capillaries (C4dPTC) has emerged as a useful method to detect antibody-mediated rejection in situ. In this retrospective study, we evaluated the prevalence of C4dPTC deposition in allograft renal biopsies diagnosed of IgA nephropathy (IgAN) and analysed its clinical significance. Method:, Sixty-six biopsy specimens of post-transplant IgAN, which were obtained to evaluate azotemia and/or heavy proteinuria, were examined by immunohistochemical staining of the paraffin sections with polyclonal antibody for C4d. Results:, C4d was stained positively in peritubular capillaries in 16 (24%) of the 66 cases. The C4dPTC -negative (n=50) and C4dPTC -positive groups (n=16) were not different in recipient gender, age, donor age, type of donor (living vs. cadaveric), interval from transplantation to graft biopsy (41.6± 21.8 vs. 48.3±26.1 months) and post-biopsy follow-up period (60.3±23.3 vs. 56.9±25.4 months). During the follow-up period, 12 of 50 (24%) although the incidence of graft failure was not different by the C4d deposition in peritubular capillaries, intervals from renal biopsy to graft failure tended to be shorter in C4dPTC -positive cases than C4dPTC -negative cases. In Kaplan,Meier analysis, the renal allograft function of the C4dPTC -positive group deteriorated more rapidly than that of the C4dPTC -negative group (p<0.05). Histologically, the C4dPTC -positive group had findings suggestive of acute cellular rejection more commonly than the C4dPTC -negative group (p<0.01). Conclusions:, Evidence of humoral rejection, as demonstrated by C4dPTC deposition, was concurrently present in significant portions of post-transplant IgAN biopsy specimens and was associated with more rapid deterioration of renal function. These results suggest that C4dPTC positivity needs to be determined at the time of biopsy even in cases of post-transplant glomerulonephritis and immunosuppression may need to be modified accordingly. [source]


Activity of CuZn-superoxide dismutase, catalase and glutathione peroxidase in erythrocytes in kidney allografts during reperfusion in patients with and without delayed graft function

CLINICAL TRANSPLANTATION, Issue 1 2006
L Doma
Abstract:, Background:, Generation of reactive oxygen species (ROS) is the main mechanism involved in the ischemic/reperfusion damage of the transplanted organ. Oxygen burst is a trigger for complex biochemical events leading to generation of oxygenated lipids and changes in microcirculation. Many markers have been researched to prove the presence of ROS in the transplanted tissue. Some of them, like superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) are considered to play a major role in graft protection against oxygen stress during reperfusion. Methods:, The aim of this study was to examine the changes of SOD1, CAT and GPx activity in erythrocytes during the first minutes after total graft reperfusion. Forty patients undergoing kidney transplantation at our center were assigned to two groups: with or without delayed graft function (DGF). Before anastomosing kidney vessels with recipient's iliac vessels, the ,0' blood sample was taken from the iliac vein. Next blood samples I, II and III were taken from the graft's renal vein. The reperfusion of the transplanted kidney was evaluated precisely with the thermovision camera. Erythrocyte SOD1, CAT and GPx activity was measured with a spectrophotometric method. Results:, We did not observe statistically significant changes in SOD1, CAT and GPx activity in erythrocytes during the early phase of reperfusion in patients with and without DGF. Conclusions:, Erythrocyte-antioxidative system in graft's vein remain stable during the early phase of reperfusion. The results of the study suggest that further studies on extracellular enzymes are required for the assessment of antioxidant system in the conditions of ischemia/reperfusion. [source]


Pediatric renal transplantation: Single center experience

PEDIATRIC TRANSPLANTATION, Issue 1 2005
Sevgi Mir
Abstract:, Although renal transplantation (RTx) is actually the first choice of treatment for children with end-stage renal disease, the number of transplanted children remains low in comparison with adults. The experience of the individual pediatric transplant center is very important in the outcome of pediatric transplant recipients. In this study, our pediatric renal transplantation experience is presented. We retrospectively analyzed the results of 72 pediatric renal transplants performed at Ege University Pediatric Nephrology Transplantation Center between June 1989 and May 2003. They were 40 girls, 32 boys and their mean RTx age was 13.27±3.73 yr (range 3,20 yr). Thirty-eight (52.8%) of the transplanted kidneys came from a living related donor, and 34 (47.2%) from a cadaveric donor. Preemptive RTx was performed in one patient and a second RTx was performed in one patient after two-period hemodialysis. Hypertension (31.9%), acute rejection (27.8%) and chronic rejection (13.9%) were the most common complications. Cytomegalovirus (CMV) infection occurred in 15 children (20.8%), none of whom died or lost their graft as a result of the infection. Pretransplant acquired hepatitis C virus (HCV) infection was detected in 12 patients (16.7%). Urinary tract infections (UTIs) were seen in 31 (43.1%) recipients. The 1, 5 and 10 yr graft survival rates were 91, 84 and 77%, respectively, and corresponding patient survival rates were 97, 84 and 77%, respectively by Kaplan,Meier method. The graft and overall survival was not correlated with sex, donor type, treatment modality, acute rejection episodes, hypertension, UTIs, CMV and HCV infection. [source]


Tissue HHV6 and 7 determination in pediatric solid organ recipients , a pilot study

PEDIATRIC TRANSPLANTATION, Issue 6 2003
M. Gupta
Abstract:, Herpes virus infections remain a major challenge in solid organ transplantation. HHV6 and 7 blood viral load was associated with pathology after renal transplantation. Little is known about the significance of tissue HHV6 and 7 infections. A total of 18 tissue biopsies (13 kidney, three GI and two BAL) from nine pediatric transplant patients (five kidney, two liver, one combined liver and kidney and one bone marrow transplant) were subjected to blood HHV6 IgG and IgM testing. In addition, tissue HHV6 and 7 semi-quantitative PCR analysis with subsequent detection by ELISA and quantitative methods were applied to the same samples. We also studied four native kidney biopsies of children with other kidney disease. The results of the biopsies were correlated with clinical data. Of the transplant patients, 78% were HHV6 IgG positive. Six of nine had a positive IgM on at least one occasion, however, only two of nine transplant patients were symptomatic with a mixed CMV/EBV septic picture of multi-organ failure. Only these two patients had a significant tissue viral load for HHV6. Additionally, a very significant tissue viral load for HHV6 was detected in an immunocompromised patient 3 wk after a roseola-like febrile illness. The HHV6 copies were 31, 88 and 206 per 10 ,L of DNA, respectively. In the patient who also had the fourth positive ELISA for HHV6 PCR product, the Multiplex PCR and restriction enzyme assay on its PCR product revealed a significant contribution by HHV7, while the HHV6-B signal was rather weak. Significant tissue HHV6 loads can be found in tissue biopsies from organ recipients with significant illness and also in native kidneys after primary infection. This may explain the high prevalence of HHV6 in transplanted kidneys. Further studies on HHV6 and 7 using molecular techniques should be supported. [source]


Renal ACE2 expression in human kidney disease,

THE JOURNAL OF PATHOLOGY, Issue 5 2004
AT Lely
Abstract Angiotensin-converting enzyme 2 (ACE2) is a recently discovered homologue of angiotensin-converting enzyme (ACE) that is thought to counterbalance ACE. ACE2 cleaves angiotensin I and angiotensin II into the inactive angiotensin 1,9, and the vasodilator and anti-proliferative angiotensin 1,7, respectively. ACE2 is known to be present in human kidney, but no data on renal disease are available to date. Renal biopsies from 58 patients with diverse primary and secondary renal diseases were studied (hypertensive nephropathy n = 5, IgA glomerulopathy n = 8, minimal change nephropathy n = 7, diabetic nephropathy n = 8, focal glomerulosclerosis n = 5, vasculitis n = 7, and membranous glomerulopathy n = 18) in addition to 17 renal transplants and 18 samples from normal renal tissue. Immunohistochemical staining for ACE2 was scored semi-quantitatively. In control kidneys, ACE2 was present in tubular and glomerular epithelium and in vascular smooth muscle cells and the endothelium of interlobular arteries. In all primary and secondary renal diseases, and renal transplants, neo-expression of ACE2 was found in glomerular and peritubular capillary endothelium. There were no differences between the various renal disorders, or between acute and chronic rejection and control transplants. ACE inhibitor treatment did not alter ACE2 expression. In primary and secondary renal disease, and in transplanted kidneys, neo-expression of ACE2 occurs in glomerular and peritubular capillary endothelium. Further studies should elucidate the possible protective mechanisms involved in the de novo expression of ACE2 in renal disease. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]


Increased Expression of Senescence-Associated Cell Cycle Inhibitor p16INK4a in Deteriorating Renal Transplants and Diseased Native Kidney

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2005
Anette Melk
Some features of kidney transplants with dysfunction overlap the lesions of aging, such as tubular atrophy and interstitial fibrosis (TA/IF) without major glomerular abnormalities. Somatic cell limitations could contribute to deterioration in aging and disease states. Since expression of p16INK4a, a cell cycle inhibitor associated with somatic cell senescence in vitro, is induced in aged kidney, we studied whether kidneys with dysfunction and TA/IF manifested increased p16INK4a expression. We performed p16INK4a immunostaining on transplanted kidneys and native kidneys with chronic renal diseases. At implantation, transplants manifested little TA/IF, and nuclear p16INK4a immunostaining was consistent with age. However, transplants biopsied for abnormal function displaying TA/IF showed strong nuclear and cytoplasmic p16INK4a staining, beyond the amount predicted for age. Both atrophic and non-atrophic nephrons displayed increased p16INK4a, suggesting that it was not simply a feature of atrophy. Epithelial p16INK4a staining was not increased in transplants with good function, but was increased in diseased native kidneys. The finding of increased p16INK4a expression in renal transplants and diseased kidneys with TA/IF and impaired function supports the concept that some cell senescence changes that accompany aging are also induced by injury and disease stresses. Thus, aging, injury and disease may share common pathways involving somatic cell senescence. [source]