Modification of hyperacute canine renal homograft and pig-to-dog heterograft rejection by the intra-arterial infusion of citrate

Hyperacute rejection was studied in seven presensitized canine recipients of renal homografts and in 22 canine recipients of pig kidneys. Under both experimental circumstances, untreated animals rejected the grafts within a few minutes. With the intra-arterial infusion of sodium citrate, hyperacute heterograft rejection was forestalled for the duration of therapy, and with homografts the benefit outlasted treatment by many hours. The protection of heterografts was not due solely to anticoagulation by the citrate, since heparin in large doses did not accomplish the same thing. A contributory factor may have been complement inhibition since removal of complement by the grafts was greatly reduced in the citrate-treated animals. © 1971

Clotting Changes, Including Disseminated Intravascular Coagulation, during Rapid Renal-Homograft Rejection

One of two patients in whom early homograft rejection developed after renal transplantation had many antidonor antibodies before operation. By the measurement of gradients across intracorporeal and extracorporeal homografts in this patient, the new kidneys were shown to sequester host immunoglobulins, platelets, white cells and clotting factors. Moreover, the renal venous blood then contained fibrinolytic activity. This presensitized recipient, as well as a second patient who did not have detectable preformed humoral antibodies, gave evidence from clinical observation and from the various clotting tests of disseminated intravascular coagulation with fibrinolysis and a severe bleeding diathesis. Immunofluorescent and histologic studies revealed a laying down of fibrin in the homograft vessels that continued in some cases to cortical necrosis of the transplanted kidneys or, alternatively, receded at the time fibrinolysis occurred. The variety of rejection seen in these patients has been characterized as an immunologically induced coagulopathy. © 1970, Massachusetts Medical Society. All rights reserved

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York