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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parameters of early failure in kidney transplantation have been analyzed from 507 transplantations with transplant loss in the first month, selected among the 7541 cadaveric kidney transplantations performed in France between 1985 and 1989. These failures represent 6.7 percent of the population transplanted over this period of time, 68.6 percent of the failures that occurred in the first 3 months post-grafting, and 47 percent of the total number of the first year failures. Comparing patients with and without transplant failure in the first month, sex of the donor and the recipient, ABO group of the donor and the recipient, origin of the kidney, cold ischemia time, HLA compatibility, dialysis duration, number of previous transplantations, showed no influence on the occurrence of early failure. Three parameters appeared to be significant risk factors: donor's age less than 5 years, P = 0.00001; recipient's age less than 5 years, P = 0.05; pregraft immunization, P = 0.002. Furthermore, multifactorial analysis showed that the absence of HLA compatibilities between donor and recipient in hyperimmunized patients also has a significant influence on early graft loss. However, comparison of these same parameters in patients with transplant failure within the first month and between 2 and 12 months post-grafting revealed that the influence of these 4 significant parameters is longstanding and that none of them is specific of the precocity of graft loss.
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PMID:[Early failure in kidney transplantation]. 183 3

1. The risks associated with nonbeneficial matching constitute a persistent hazard to the transplant over a long period. 2. The benefits of HLA matching and CsA are separate and additive. 3. There is no evidence that beneficial matching is not relevant to all (UK) centers. 4. Contemporary typing methods are expected to improve the accuracy of typing and reduce kidney cold-ischemia times. 5. Organ sharing increases the numbers of beneficial matches. 6. Patients with easily matchable ABO-HLA phenotypes should wait for beneficially matched transplants. 7. Patients with phenotypes that are difficult to match should be intelligently mismatched after due consideration of responder status, acceptable mismatches, and cross-reactive groups. 8. Organ sharing does not prejudice graft survival. 9. Wastage is minimized with a central clearing house. 10. Organ sharing reduces the incidence of high sensitization. 11. Organ sharing is cost effective. For these reasons we repudiate the view that organ sharing is now superfluous.
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PMID:In defense of organ sharing in kidney transplantation. 315 14

In a group of 276 consecutive liver transplants 8 primary graft nonfunctions were identified (2.9%). Recipients showed a progressive elevation of transferases (mean maximum value ALT: 5000 +/- 1892 U/l) and bilirubin (mean maximum value: 20 +/- 11.8 mg/dl) and a decrease in the percent prothrombin time (mean minimum value 26 +/- 13 min.) in the post-implantation survival time of the 8 grafts (range 1-5 days). No statistically significant differences were observed between mean cold and warm-ischemia times for these 8 donor organs and those of a control group of 92 consecutive grafts. All organs except one were ABO isogroup and all except another one displayed negative lymphocytotoxic crossmatch. Predominantly small-droplet hepatocytic vacuolization with no nuclear displacement was observed in plastic-embedded semithin sections of all post-primary nonfunction liver tissues (severe in 4 grafts, centri-mediozonal in 2, and centrolobular in 2). In 3 cases where fresh liver tissue was available the lipidic nature of the vacuoles was confirmed with electron microscopy and with frozen sections stained with Sudan III. Other microscopic lesions were also observed: spotty monocellular coagulative necroses, variable extension of zonal coagulative necroses and hemorrhages, cholestasis and minor mixed inflammatory infiltrate. Comparative microscopic study of these tissues with the protocol biopsy specimens obtained 2-4 hours after reperfusion demonstrated previous liver cell-vacuolization in only 3 cases. In conclusion, an acute progressive microvascular steatosis developed in this primary nonfunction series. No specific etiopathogenic factors were identified.
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PMID:A clinopathologic review of 8 liver graft primary nonfunctions. 759 May 68

Sclerosing cholangitis defined by cholangiographic criteria may occur after orthotopic liver transplantation. In this retrospective study, we analyzed failed grafts and antecedent serial biopsies of 24 patients who developed this type of nonanastomotic biliary strictures. Sclerosing cholangitis was histologically diagnosed if there was a combination of periductal fibrosis and features of large bile duct obstruction. The condition was observed in all but one available failed allografts. This later showed ischemic-type lesions without periductal fibrosis. Liver biopsy specimens were nondiagnostic relative to sclerosing cholangitis, although 85% of the patients had evidence of large bile duct obstruction. Numerous associated factors may explain the pathogenesis of secondary sclerosing cholangitis: an immunologically related etiologic factor (10 recipients of ABO-incompatible allografts) and compromised arterial blood flow that likely resulted from hepatic artery thrombosis (12 patients), focal arterial fibrointimal hyperplasia (three patients), chronic ductopenic arteriopathic rejection (three patients) and/or preservation-related ischemia (four patients). Sclerosing cholangitis may be a significant cause of graft failure that often has misleading biopsy manifestations. From a practical standpoint, cholestasis with evidence of large bile duct obstruction warrants cholangiographic assessment of the biliary tree.
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PMID:Sclerosing cholangitis following human orthotopic liver transplantation. 780 40

The aim of this study was to analyze the donor risk factors associated with second orthotopic liver transplantation (reOLT) and graft loss after OLT within 1 month. A total of 649 OLTs performed in 11 centers in Spain during the period from 1992 to 1993 were analyzed retrospectively. Eleven donor and recipient variables were studied. Biochemical evolution of the OLT, biliary and arterial complications, patient status (alive, retransplanted, or dead), and follow-up were also recorded. Bivariate study demonstrated that extended preservation ( > 12 hr) was associated with increased biliary complications (P = 0.02), and lower prothrombin time (P = 0.04). In a logistic model regression for biliary complications, ischemia > 12 hr was an independent risk factor (odds ratio = 2.2, 95% confidence interval [CI] = 1.1-4.3). The multivariate Cox proportional model of potential risk factors showed that only urgent reOLT (relative risk [RR] = 2.7, 95% CI = 1.4-5.4) was independently associated with higher 30-day mortality. Donor plasma sodium > 155 mmol/L (RR = 1.4, 95% CI = 1.0-2.2) and incompatible ABO graft (RR = 3.2, 95% CI = 1.3-7.9) were independently associated with increased rate of reOLT before 30 days. Donor plasma sodium > 155 mmol/L (RR = 2, 95% CI = 1.1-3.6) and incompatible graft (RR = 3.3, 95% CI = 1.4-8.2) were independently associated with graft loss (death or reOLT) before 1 month. We conclude that cold ischemia should be kept less than 12 hr in order to avoid biliary complications. Donors over 60 years old or with plasma sodium > 155 should be carefully evaluated before OLT.
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PMID:The deleterious effect of donor high plasma sodium and extended preservation in liver transplantation. A multivariate analysis. 861 Mar 52

Severe hemolysis and graft ischemia complicating solitary pancreas transplantation with an ABO-compatible, Rh-negative, anti-D-positive donor to Rh-positive recipient is described in this article. A brief review of the literature is presented. A rationale for preoperative screening for red cell antibodies during solid organ transplantation in this special setting is discussed.
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PMID:Humoral graft-versus-host disease after pancreas transplantation with an ABO-compatible and Rh-nonidentical donor. Case report and a rationale for preoperative screening. 862 9

Overall one-, 5-, and projected 10-year graft survival rates were 81%, 58% and 39%, respectively for 51,442 cadaveric kidney transplants performed at 251 U.S. transplant centers from October 1987-December 1994. The comparable results for recipients of living donor kidneys were significantly higher, 91%, 75%, and 60% (p<0.001). One-year first cadaver graft survival rates improved from 77% for transplants performed in 1987-1988 to 84% for transplants performed in 1991-1992 (p<0.001). Recipients of second cadaveric transplants in 1987-1988 had a 69% one-year graft survival rate compared with 81% for those transplanted after 1990 (p<0.001). Graft survival rates have been stable since 1991. The percentage of broadly sensitized first transplant recipients decreased from 13% before 1991 to 7% after, and the one-year graft survival rates increased by 4-6% for both sensitized and nonsensitized recipients between the 2 periods (p<0.001). Among retransplanted patients, the percent of broadly sensitized recipients fell from 40-33% over the same periods (p<0.01). One-year graft survival rates increased by 7-8% for sensitized and nonsensitized patients (p<0.001). One-year graft survival rates improved from 74-83% for Blacks (p<0.001) and from 78-85% for non-Blacks (p<0.001) transplanted for the first time when comparing transplants performed in 1987-88 with those performed in 1993-94. The cause of donor death had a significant effect on graft survival. The 5-year graft survival rate was 61% for 28,923 recipients of trauma donor kidneys compared with 54% for 16,956 transplants from CVA donors (p<0.001). Kidneys from CVA donors increased from 28% of all cadaveric kidneys in 1988 to 38% in 1994. The donor's age was a more important determinant of long-term survival, however, and correlated strongly with the cause of donor death. Only 16% of CVA donors were reportedly age 30 or less, compared with 75% of trauma donors. First cadaver graft survival decreased by approximately 2% for each 12 hours of cold ischemia time. Although there was a significant increase in the incidence of delayed graft function from 19% when the CIT was less than 12 hours to 35% when the CIT was more than 36 hours, there was no significant long-term effect of cold ischemia time. The recent change in UNOS policy to share zero-HLA mismatched kidneys resulted in a 2-fold increase (from 8%-16%) in the number of HLA-matched transplants performed during the first 6 months following the change. The percentage of Blacks who have received matched kidneys following this change has increased from less than 2% to more than 5%, a 3-fold increase. The 163 Blacks who received an HLA-matched kidney prior to 1995 had a 65% 4-year graft survival rate compared with 53% for mismatched Blacks (p<0.001). The incidence of early rejections was also reduced by 25% among matched recipients and the graft half-life was 8 years compared with 5 years for mismatched Blacks. About 25% of HLA-matched kidneys were transplanted to ABO compatible but not identical recipients. Although the effect of the policy allowing compatible transplants did not result in a large number of type O kidneys transplanted to non-O recipients when only 8% of kidneys were shared, the recent change in allocation policy may be detrimental to type O waiting patients.
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PMID:The UNOS scientific renal transplant registry. United Network for Organ Sharing. 879 51

Liver regeneration in a patient with fulminant hepatic failure (FHF) who underwent living-related partial liver transplantation (LRLT) was investigated regarding hepatic growth factors. The patient was a 16-yr-old Japanese male who developed severe subacute FHF. LRLT was performed using an extended left lobe of the ABO matched patient's mother. In the recipient, the pre-transplant levels of both plasma hepatocyte growth factor (HGF) and transforming growth factor (TGF)-beta were extremely high and rapidly decreased following the liver replacement. The liver volume evaluated using a CAT scan increased 195% after 2 wk in graft liver and 110% after 2 wk in the hepatectomized donor. The explanted liver (FHF liver), the liver from donor (normal liver), and the graft liver [the 3rd post-transplant day (POD 3)] were all investigated immunohistochemically. FHF liver: No liver regeneration was observed [proliferative cell nuclear antigen (PCNA) labeling index (L.I.): 0%]. In the liver, both HGF in the hepatocytes and c-met on the membrane of the hepatocytes were positive. TGF-beta was positive in the hepatocytes and no apoptosis was detected by the TUNEL method. Donor liver (POD 0): Few PCNA stained hepatocytes were detected. No HGF was detected but c-met was clearly detected on the cell membrane of the hepatocytes. Neither TGF-beta nor apoptosis was detected. Graft liver (POD 3): The PCNA L.I. was conspicuous at 40%. HGF was positive in non-parenchymal cells and c-met was positive in the cytoplasm of the hepatocytes. TGF-beta was negative while apoptosis was positive in the zone 3 hepatocytes. In conclusion, these findings suggested that the liver of the patient with FHF did not respond to liver regenerative stimulus, in part, through involvement of inhibitor TGF-beta. On POD 3, the transplanted graft was in a vigorous regenerative status in comparison to that in the hepatectomized donor. The HGF/c-met system is thought to be involved in the mechanism of regeneration. Intrahepatic apoptosis was detected in the graft on the 3rd post-transplant day probably due to transient ischemia in the liver, which was not related to the Fas/Fas-ligand system.
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PMID:Changes in liver regenerative factors in a case of living-related liver transplantation. 1061 46

Between June 1990 and August 1997, 304 mainly pediatric patients underwent a total of 311 orthotopic living related liver transplantations (LRLTs) under tacrolimus immunosuppression at Kyoto University Hospital. Congenital biliary atresia was the most common underlying disease. The donor was a parent, and the left lateral segments were used as grafts in most cases. The average number of loci of HLA-A, -B, and -DR mismatches between the donor and the recipient were 2.1. Forty-three transplants were ABO-incompatible. Liver histology at the time of abnormal liver function after transplantation was analyzed. Preservation injury was rare and mild. Acute cellular rejection (ACR) occurred in 36% of transplants during the first 6 months. Average rejection activity index (the Banff schema) was 4.2 and severe rejection was rarely seen. The number of mismatching HLA loci and immunosuppression regimens affected the incidence of ACR. Chronic rejection (CR) occurred in 2% of transplants. Concerning humoral rejection, no hyperacute rejection was seen. However, hepatic artery thrombosis (delayed hyperacute rejection) was seen in an ABO-incompatible transplant. Acute hepatitis, including those related to cytomegalovirus and Epstein-Barr virus, occurred in 17% of transplants. Chronic hepatitis, including hepatitis B and C, developed in 3%. Acute or chronic cholangitis occurred in 16%, and a significantly higher incidence of cholangitis was found in ABO-incompatible transplants. Posttransplantation lymphoproliferative disease developed in 2%. In LRLT, milder preservation injury and less frequent ACR and CR were suggested, probably because of the short cold-ischemia time and the advantages of HLA histocompatibility, respectively.
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PMID:Living related liver transplantation: histopathologic analysis of graft dysfunction in 304 patients. 1066 27

Primary non-function (PNF) of renal allografts has been attributed to various risk factors, among them immunological ones, as well as unfavourable preservation conditions. To investigate the impact of these risk factory on the occurrence of PNF, 1335 consecutive kidney transplants performed at a single centre over a 10-year period were analysed. All patients received immunosuppression based on cyclosporine. As the method of analysis a conditional stepwise logistic regression model was chosen, comparing each graft suffering PNF with its partner kidney retrieved from the same donor. Thus, all donor-related variables could be omitted from the analysis, as they are the same in every pair of grafts. Risk factors analysed included panel-reactive antibodies, number of pretransplant transfusions, pregnancies, number of prior transplants, cold and second warm ischaemia time, mismatches on HLA loci A, B and DR and recipient age. The overall incidence of PNF was 87 grafts (6.5%). One patient suffered immediate rejection due to transplantation of an ABO incompatible graft. This case was excluded from further analysis. PNF occurred three times in recipients of living related grafts, twice in recipients of en-bloc grafts and four times in grafts, in which the paired kidney was either not transplanted or shipped outside the Eurotransplant region, so that no paired graft was available for matched case-control analysis. Of the remaining 77 pairs, twice both organs of one donor failed immediately. The remaining 73 complete pairs were analysed. Two of the investigated risk factors have independently a significant impact on the occurrence of PNF. Increasing the number of pretransplant transfusions raises the relative risk of graft failure up to six fold (P=0.02), while a history of prior transplants bears a relative risk of 0.21E05 (P=0.005). Ischaemia has no significant impact on the occurrence of PNF. Our data strongly suggest that immunological rather than donor risk factors are responsible for the non-function of kidney grafts.
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PMID:Immunological risk factors are solely responsible for primary non-function of renal allografts. 1127 Dec 29


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