Transfusion effect in renal transplants.
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Biomedical subjects
Publications and source records attributed to B K Shenton.
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Twenty-three human cadavers kidneys were studied during hypothermic pulsatile perfusion prior to transplantation. The accumulation of laevo-lactate and lactate dehydrogenase, alterations in pH and perfusion flow rate were measured and compared with organ function following transplantation. No parameter measured was found to be an accurate index of potential function.
Over the past few years many centres have shown that blood transfusions given to potential renal transplant patients are beneficial to subsequent graft survival. Results from this centre have shown that an elevated ability of plasma to suppress lymphocyte reaction to antigen is associated with blood transfusions in chronic renal failure patients. In a prospective study, plasma suppressive activity was measured at the time of transplantation in 49 patients who were followed for between 3 and 15 months. Results showed that patients with a low level of plasma suppressive activity were at risk from early graft loss due to acute rejection. Furthermore, most of the suppressive activity was related to the naturally occurring plasma protein. alpha 2-macroglobulin. This prospective study reports a significant association between low plasma suppressive activity and early kidney graft loss through rejection, and suggests an explanation for the beneficial effects of blood transfusion on graft survival.
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Blood transfusions given to potential renal transplant recipients are beneficial to subsequent graft survival. This study has shown an association graft survival. This study has shown an association between the inhibitory activity of patients' plasma on their own non-specific lymphocyte responses to antigen and the administration of blood transfusions. Most of the inhibitory activity was related to alpha-2 macroglobulin. Alpha-2 macroglobulin was able to prolong the survival of rat cardiac allografts. Immunoregulatory activity related to the alpha globulins of plasma has been described in a wide variety of conditions (i.e. cancer, pregnancy, diabetes) and this study has shown similar activity following blood transfusions.
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A combined familial study of multiple sclerosis (MS) in England and in the Rostock area of the GDR using the macrophage electrophoretic mobility (MEM)-LAD test embracing 132 relatives has revealed a closely similar pattern of distribution of "anomalous" LAD (Linoleic Acid Depression) values in relatives (77% type of reaction) to that originally reported in the British study. The anomaly in predominantly associated with females--all mothers of MS patients being affected, whilst daughters and sisters are also represented. In addition unusual full MS type of reaction (90% reduction) has been found in some children related to patients. There is clearly a genetic element in the development of MS probably mainfested in the inborn mishandling of unsaturated fatty acids suggested by Thompson; no recognizable pattern of inheritance is noticeable even within the combined material. There is evidence that the metabolic anomaly alone does not inevitably lead to MS, and the full abnormality may be present at an early age. A survey about the examinations and a selection of characteristic family trees of MS are given, illustrating the manner in which the 77% type anomaly is distributed with occasional omission of a generation.
In this study the macrophage electrophoretic mobility (MEM) test was modified by using tanned sheep erythrocytes in place of guinea pig peritoneal macrophages as the indicator cells of lymphocyte sensitization to antigens. This modification is named the tanned sheep erythrocyte electrophoretic mobility (TEEM) test, and a comparison of the kinetics of the two systems allowed the following conclusions to be made: 1) Treatment of freshly drawn sheep red blood cells with a concentration of 1/40,000 tannic acid produced optimum results in the TEEM test. 2) Lymphocyte-antigen and lymphocyte-number response curves show similarity in the two test systems. 3) A plateau response with slowing factor is achieved at a lower dilution in the TEEM test than in the MEM test. 4) Whilst similarity in the first stage reaction was found in the two systems, in the second stage of the test (at 37 degrees C) tanned sheep red cells gave a plateau response after 45 min instead of the 60 min found in the MEM test. 5) The two slowing factors showed similar gel filtration patterns with molecular weights between 13,000 and 15,000 daltons, and had equivalent activity in both test systems. 6) The disadvantages of the guinea pig macrophage as an indicator cell are discussed. 7) The TEEM test seems simpler to perform than the MEM test and may be widely applicable in clinical immunology for the estimation of lymphocyte sensitization.
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The mixed lymphocyte reaction (MLR) as measured by the macrophage electrophoretic mobility (MEM) test is markedly reduced between unrelated multiple sclerosis (MS) patients. This is not the case with other neurological diseases (OND). Within an MS family, the MLR between the propositus and members of the family falls into the low (MS type) range or into the normal or OND range. Those members who give the low results are those who have a MEM-LAD test result of about 77 per cent, i.e. halfway between that of normal and MS. There is thus a parallelism between the anomalous response to linoleic acid and an unexpectedly low MLR with known MS lymphocytes. Lymphocytes from apparently normal children who have a high (MS-type) linoleic acid depression result take part in an MLR with MS cells, as if they were themselves true MS cells. Some possible implications these findings may have for the pathogenesis of MS are discussed.
Lymphocyte sensitization to measles has been studied in comparable groups of multiple sclerosis, other neurologic disease and normal subjects. The macrophage electrophoretic mobility test has been used. No difference between the three groups has been found, though there is a small group of children with obscure neurological disease which might well be multiple sclerosis and which fails to mount an adequate response to measles. The role of measles (and other banal infections) in aetiopathogenesis of multiple sclerosis is briefly discussed.
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