PubMed · 7233524
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P D Mintz. More type and screen.. https://doi.org/10.1046/j.1537-2995.1981.21381201817.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND: The Rh (D) blood group system has not traditionally been considered to be a clinically relevant histocompatibility barrier in transplantation since conflicting results of its clinical importance have been reported. METHODS: We analyzed 786 consecutive primary cadaveric renal transplants performed by transplant centers in our Organ Procurement Organization (OPO) between 1990 and 1997. We also analyzed United Network for Organ Sharing (UNOS) data on 26,469 kidney transplants done from April 1994 to June 1996. RESULTS: Multivariate analysis revealed that Rh identity between the recipient and donor was significantly related to better graft outcome (risk ratio, 0.43; 95% confidence interval, 0.30 to 0.61; P=0.0001). Multivariate analysis of the UNOS data revealed that the Rh -/- group may have a positive influence on graft survival with a risk ratio of 0.43 (P=0.14). CONCLUSION: Multivariate analysis of primary cadaveric renal allografts performed within the Midwest Organ Bank OPO indicates that Rh (D) is a clinically relevant histocompatibility barrier that influences 7-year graft survival.
BACKGROUND: Because of the numerous risks associated with the use of packed red blood cells (RBCs), it is critical that they be transfused only when appropriate. A hospital-wide educational program was developed in an attempt to improve the transfusion practices and provide a framework for blood bank audit at a Veterans Affairs teaching hospital. MATERIALS AND METHODS: The program required physicians to fill out an information sheet that listed appropriate criteria for transfusion. Charts were reviewed to determine if the transfusion met these criteria. If the transfusion was deemed inappropriate by peer review, the staff physician was notified by letter. The information sheet was used on a voluntary basis without chart review in 1989 and on a mandatory basis beginning in 1990. Transfusion rates and mortality were adjusted to patient days of hospitalization and evaluated using chi 2 analysis. RESULTS: While voluntary use did not affect transfusion rate, mandatory implementation resulted in a 26% decline (P < 0.001) between 1989 and 1990 in the number of RBC units transfused per patient days of hospitalization. A diminished use of RBCs persisted in the subsequent years. There was no increase in mortality during this time to suggest a detrimental effect from the decrease in RBC transfusion. No apparent variation in the hospital population could account for the changes. CONCLUSION: Use of a unique and simple transfusion request sheet as an educational tool resulted in improved transfusion practices at a Veteran Affairs teaching hospital.
OBJECTIVE: To determine the fetal Rhc genotype by using the polymerase chain reaction (PCR) amplification procedure and maternal blood at the different steps of the fetal cell enrichment process. METHODS: Maternal peripheral venous blood samples were obtained from 11 pregnant women homozygous for the C antigen before amniocentesis. Three were not alloimmunized and eight were alloimmunized. The fathers were known to be heterozygous or homozygous for the c antigen by serologic testing. The mononuclear cell layer was isolated from maternal blood and flow sorted using monoclonal antibodies to CD36 or CD71 and glycophorin A. This was followed by PCR of the blood, mononuclear cells, and the sorted cells with allele-specific primers to RhCc genes. Gel electrophoresis was performed to predict fetal Rhc genotype. The fetal RhCc genotype was confirmed by serologic and DNA testing. RESULTS: All infants were positive for the Rhc gene. The positive fetal Rhc genotype was determined correctly in three of the 11 maternal blood samples without enrichment, in six of the nine mononuclear cell samples, and in seven of the eight sorted cell samples. The fetal genotype from one sorted sample was predicted to be homozygous C. One infant was determined by serology on cord blood to be negative for the c antigen, but repeated infant DNA amplification was consistent with the c genotype. CONCLUSION: Noninvasive fetal Rhc genotyping can be determined by PCR amplification of the rare fetal cells in maternal blood. These data reaffirm that enrichment of maternal blood for fetal cells is necessary to improve the sensitivity of the test.