Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous experimental and human data suggests a detrimental effect on the course of acute renal failure related to exposure of blood to artificial dialysis membranes of poor biocompatibility. We performed a 2.5-year prospective randomized trial to compare the clinical course of acute renal failure (post-operative ischemic acute tubular necrosis, ATN) in patients receiving a cadaveric renal transplant requiring supportive hemodialysis in the immediate post-transplant setting. Patients were randomized to either a cuprophane or polymethylmethacrylate (PMMA) conventional hollow fiber dialyzer. All patients received a standard immunosuppressive regimen which included induction therapy with either horse anti-thymocyte gamma globulin (ATGAM) or the murine anti-CD3 monoclonal antibody (OKT3). Of 53 patients randomized, 17 were excluded (2 for intervening biopsy-proven rejection prior to recovery from ATN, 10 for primary graft nonfunction and 5 for other reasons), leaving 36 evaluable cases of uncomplicated ATN, 18 in each group. There was no difference by age, race, gender, cause of ESRD, immunosuppressive regimen, cold or warm ischemia time, use of pre-transplant dialysis, percent oliguria or the incidence of intra-dialytic hypotension between the 2 groups. There was no difference in the mean time to recovery from ATN posttransplant (8.9 days in the cuprophane group vs 9.5 days in the PMMA group, p = NS) or in the average number of hemodialysis treatments required (3.6 in both groups, p = NS). There was also no difference in long term allograft outcome in terms of the nadir serum creatinine, the number of episodes of subsequent acute rejection or in the development of chronic rejection. An intent-to-treat analysis of all 53 originally randomized patients similarly yielded no significant differences. A subsequent, non-randomized study using a membrane of intermediate biocompatibility (Hemophan) also showed no difference in recovery time from ATN. Bioincompatible membranes do not seem to have a significant clinical impact on the course of recovery of this form of acute renal failure. The striking benefits of biocompatibility in the course of ARF seen in other human trials may relate more to the non-renal systemic toxic effects of bioincompatibility.
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PMID:Biocompatible dialysis membranes and acute renal failure: a study in post-operative acute tubular necrosis in cadaveric renal transplant recipients. 898 57

Rupture of a renal allograft (RAR) is an uncommon but serious complication of renal transplantation. A recent RAR prompted a review of our experience, with the purpose of (1) identifying conditions that may predispose this complication and (2) defining strategies for prevention. A 5-yr, consecutive living-related (LRD) and cadaver donor (CD) cohort of 331 patients was studied retrospectively. Twelve patients (3.6%) had RAR. Donor characteristics, procurement and preservation conditions, and recipient characteristics were major study categories. Data analysis was computer-based and included multivariate analysis. The nine White and two Black cadaver donors were "ideal", mean age 29 yr, with mean high creatinine (CR) of 1.3 and terminal CR of 1.1 mg/dl and mean terminal urine output of 423 ml/min. Nine of 11 CD had low-dose dopamine use (terminal, mean 8, range 5-13 micrograms/kg/min). Eleven of 11 donors had procurement en-bloc, 9 of which were multiple organ procurement. All had 4+/4+ flush and cold storage with UW solution. Mean cold ischemia time (CIT) was 22 h, 28 min (range 15 h, 16 min to 40 h). For patients with RAR mean age was 39 yr; there were 12 Black patients and 7 males, 5 females. HLA match was 1 antigen (AG) for 3, 2 AG for 8, and 4 AG for 1 (mean 1.9). Nine patients had delayed or declining renal function requiring dialysis. The panel reactive antibody was at peak, mean 47% (range 0-100%) and current, mean 18% (range 0-84%). Six of 12 had OKT3 therapy at time of RAR and six had biopsies. Day of RAR was mean 10, median 9 (range 4-21). Pain and drop in hematocrit were observed in most. There was one fatality (8%), and all kidneys were removed. All kidneys showed at least minimal rejection but six had severe acute tubular necrosis (ATN) with edema and minimal rejection. Statistically significant associations with RAR were older recipient age (p = 0.01), donor-recipient race mismatch (White donor to Black recipient) (p = 0.007), and dialysis requirement (p < 0.001). Other variables were not statistically correlated: gender, race, CIT, transplant number, LRD vs. CD, peak or current PRA, and total HLA and BDR mismatch. The data suggest that ATN and rejection act synergistically to cause RAR and that early delayed function requires intensive and perhaps novel immunosuppression, especially in Black recipients.
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PMID:Renal allograft rupture: a clinical review. 899 57

Experimental preservation time for pulsatile perfused dog kidneys was extended from three to five days by phospholipase A2 inhibition suggesting a pathomechanical role of products of phospholipolysis like thromboxane and leukotrienes in the development of acute graft failure after renal transplantation. We therefore investigated the effects of thromboxane- and leukotriene synthase inhibitors on postoperative renal transplant function in a model of pulsatile perfusion preservation as well as a cold storage preservation of dog kidneys. Addition of a thromboxane-synthase-inhibitor to the perfusion medium in pulsatile perfused kidneys and the combined application of a thromboxane-synthase-inhibitor and a leukotriene-synthase-inhibitor to the recipient of a cold storage preserved graft, improved graft function and reduced the incidence of delayed graft function as well as histopathological features of acute tubular necrosis.
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PMID:Long-term renal preservation and prevention of acute tubular necrosis by inhibition of arachidonate metabolism. 912 38

Vascular thrombosis remains a major cause of graft failure, accounting for 12.2% of failed index transplants and 19.2% of repeat transplants. We conducted a special study to identify the risk factors for vascular thrombosis. A total of 4394 transplants (2060 living donor [LD] transplants and 2334 cadaver donor [CAD] source transplants) were evaluated. The respective vascular thrombosis rates for LD and CAD transplants were 38/2060 (1.8%) and 100/2334 (4.2%) (P<0.001). Univariate analysis showed that the rate of graft loss due to thrombosis was significantly higher in younger children (less than 2 years of age) as compared with older age groups (2-5 years, 6-12 years, and more than 12 years of age) (9.0% vs. 5.5%, 4.4%, and 3.5% for CAD transplant recipients and 3.5% vs. 3.4%, 0.7%, and 1.9% for LD graft recipients). Recipients of kidneys from cadaver donors less than 5 years of age had a significantly higher thrombosis rate (8.3%) than did recipients from older donor groups (5-10 years, 4.5%; greater than 10 years, 3.2%). Recipients of kidneys with cold ischemia time greater than 24 hr also had a higher thrombosis rate (5.6%), as compared with recipients of kidneys with a shorter cold ischemia time (3.2%). Recipients of antilymphocyte therapy on day 0 or day 1 were at dimished risk of graft loss due to thrombosis (2.2% vs. 4.1%, P=0.001). Comparable trends were seen for both LD and CAD organ recipients. LD organ recipients with a history of prior transplantation had a significantly higher rate of thrombosis as compared with those who received a primary transplant (4.6% vs. 1.6%, P=0.005). For both LD and CAD organ recipients, the occurrence of acute tubular necrosis was a significnat risk factor for the development of thrombosis. Regression analysis showed that for LD organ recipients, a history of prior transplantation increased the risk for thrombosis, whereas increasing recipient age had a linear decreasing risk effect. The use of antilymphocyte antibody or cyclosporine on day 0/1 decreased the risk for thrombosis. For CAD kidney recipients, organ cold ischemia time greater than 24 hr increased the risk for thrombosis. The use of antibody induction therapy, donors greater than 5 years of age, and increasing recipient age were factors that decreased the risk for thrombosis.
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PMID:Risk factors for vascular thrombosis in pediatric renal transplantation: a special report of the North American Pediatric Renal Transplant Cooperative Study. 915 19

The purpose of this study was to determine whether use of vasopressors in cadaveric donors of renal transplants was associated with an increased prevalence of acute tubular necrosis after kidney transplantation. We compared immediate allograft function in 26 consecutive renal allograft recipients whose donors had been given vasopressors with that in 26 recipients whose donors had nor. The donors treated with vasopressors had been given more than 10 micrograms/kg per minute of dopamine, norepinephrine, or epinephrine, alone or in combination. The groups were matched with respect to donors' age, recipients' disease, and cold ischemic time. The prevalence of immediate allograft function was significantly lower in recipients whose donors had required use of vasopressors (38.5%) than in recipients whose donors had not required vasopressors (65.4%). We conclude that use of vasopressors in kidney donors leads to an increased prevalence of acute tubular necrosis.
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PMID:Effect of use of vasopressors in organ donors on immediate function of renal allografts. 918 88

Acute tubular necrosis (ATN) is a common condition of following cadaveric renal transplantation with an incidence in many series of nearly 50%. The aetiology is uncertain; however, it would appear to be related to damage to the transplant kidney either prior to retrieval, During cold preservation or during re-warming of the kidney at the time of anastamotic construction. There is no specific therapy for ATN and treatment is comprised of an expectant policy with supportive dialysis and fluid restriction. Renal function improves in the majority of cases, though there may be delayed function for several weeks. We report a case of dialysis-dependent ATN that had persisted for 5 months following transplantation. Following conversion to tacrolimus there was immediate improvement in renal function, and after a month of tacrolimus therapy the patient was dialysis-independent.
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PMID:Conversion from cyclosporin to tacrolimus in a patient with prolonged acute tubular necrosis. 928 8

"Zero-hour" biopsies of 65 donors have been performed since 1994. Donor kidneys were categorized into five groups based on the morphological findings in "zero-hour" biopsies. No morphological abnormalities were found in 38% of the cases (group 1). Arteriosclerosis was present in 31% of donor kidneys (group 2). Specific morphological alterations, i.e. acute tubular necrosis [21.5%], tubulointerstitial nephritis [6.2%] or glomerulonephritis [3.1%] were detectable in the cases remained (group 3-5). During an average of 336 posttransplant days clinical and histological follow up was performed (50 rebiopsies). Statistical data of mismatch (1.4-2.0), average of donor/recipient age (35-42 years), cold and warm ischaemic time (1290 and 66 min) were comparable in all groups. According to our observations: 1. higher creatinin was found in grafts with arteriosclerosis (group 2) (p < 0.05), 2. there were more non-viable grafts and longer period of delayed graft function in acute tubular necrosis (group 3), 3 higher creatinin, rejections with the need of rehemodialysis were observed in four cases of tubulointerstitial nephritis (TIN-group 4). Glomerulonephritis (GN-group 5) grafts had only delayed graft function, however these groups were few for statistical evaluation. Biopsy complication in 1/115 cases was found (rebiopsy induced kidney haemorrhage). In conclusion, "zero-hour" biopsies can be useful and safe tools to predict early graft function. Besides "zero-hour" biopsies help the histological interpretation of consecutive graft rebiopsies.
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PMID:Predictive morphological findings in "zero-hour" biopsies of renal allografts. 940 97

Improving organ preservation techniques for transplantation is one of the most important goals of transplantation research. We have established a new, nonfreezing cryopreservation method to optimize the viability of rat kidneys for transplantation with up to 4 M dimethylsulphoxide (DMSO) in EuroCollins solution (EC) at -5 degrees C to -15 degrees C. We have confirmed the occurrence of a tubular and glomerular defect pattern that mediates acute tubular necrosis (ATN) and that may be a cause of major histocompatibility complex (MHC) independent immunological components of chronic transplant rejection. The extent of this defect [transplant survival and function, 31P-NMR spectroscopy, histological defect index] in the nonfreezing cryopreserved groups (n = 22) is significantly (P = 0.017) lower than in the simple cold storage group (n = 12). Quality and localization of the lesions in kidney transplants can elucidate the context of organ preservation, progressive hyperfiltration defects, and the occurrence of graft failure without elevated frequency of acute rejection episodes. These results indicate that further efforts to provide higher pretransplant organ viability without using it to prolong cold storage intervals may provide better insight into MHC-independent factors of chronic transplant failure and may result in improved long-term transplant outcome.
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PMID:Nonfreezing cryopreservation--a possible means of improving long-term transplant function? 956 79

We report a 27-year-old Japanese man who developed acute renal failure associated with cold water immersion. The clinical course was consistent with that of acute renal failure attributable to acute tubular necrosis. A renal biopsy specimen showed patchy and focal loss of tubule cells, necrotic epithelium, interstitial edema, and arterial lumina obstructed by diffuse and severe intimal thickening. Endothelin increased more than five times in the early phase of the clinical course. Vasoconstriction and ischemia induced by cold exposure seem to lead to endothelin release. Endothelin may be related to the development of acute renal failure and intimal thickening.
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PMID:Acute renal failure in accidental hypothermia of cold water immersion. 959 Jan 98

Previous studies aimed at identifying the causes, risk factors, and outcome of kidney transplant recipients with delayed graft function (DGF) have yielded controversial results. We retrospectively analyzed the causes and risk factors for DGF in 263 cadaveric kidney transplantations from November 1988 to March 1997 in one center. Causes of DGF were assessed by postoperative graft evolution and graft biopsy. Univariate and multivariate analysis were used to investigate the risk factors for DGF induced by acute tubular necrosis (ATN). Seventy-six patients (29%) had DGF, which was caused by ATN in 70 patients (92.1%) and acute rejection (AR) in 6 patients (7.9%). Therefore, we focused on risk factors and consequences for ATN-induced DGF. In monofactorial analysis, ATN was significantly associated with greater weight and presence of an atheromatous disease in both donor and recipient. Other risk factors for ATN were older age of donor, recipient American Society of Anesthesiology (ASA) physical status category IV, cold ischemia time (CIT), and transplantation using the right kidney. The multivariate analysis showed that donor and recipient weight, donor age, transplantation using the right kidney, preservation in Eurocollins solution, ASA score, and CIT were associated with ATN. The incidence of rejection and renal function were not different at 3 months or 1 and 5 years. ATN is the main cause of DGF in kidney transplant recipients. ATN is caused by donor and recipient vascular background, grafting the right kidney, and CIT. ATN does not appear to have an adverse effect on long-term kidney function.
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PMID:Posttransplantation acute tubular necrosis: risk factors and implications for graft survival. 985 14


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