Optimization of Calcineurin Inhibitor Treatment after Solid Organ Transplantation

Abstract

On December 23, 1954, Ronald Herrick donated a kidney to his identical twin brother Richard who was dying of renal failure. The kidney transplant produced urine immediately and in February 1955, Richard Herrick was discharged from hospital. He survived for another nine years (at which time his kidney allograft failed from recurrent glomerulonephritis), married the nurse who attended him, became father of two children and returned to work as a radio and television engineer. His brother Ronald lived on for more than 50 years after donating his kidney.1-3 In the years following this first successful human kidney transplantation, several more kidney transplants were performed between identical twins. Most of these patients had a return of normal kidney function and survived for a considerable period of time.4 However, it was clear from previous experience that if kidney transplantation was to be extended successfully to genetically non-identical individuals, suppressing the recipient’s immune system was necessary in order to prevent acute rejection. Early after World War II, a small number of human kidney transplantations had been performed in Europe and the United States. The recipients had received no immunosuppression except for a few cases in which short courses of ACTH or cortisone had been given. Although some of these kidney allografts did function for a limited period of time -most likely as a result of profound uremia5- most of the transplanted kidneys were acutely rejected or destroyed as a result of thrombosis or infection, and none of the recipients survived for a long period of time