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MINERVA UROLOGICA E NEFROLOGICA

A Journal on Nephrology and Urology


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Minerva Urologica e Nefrologica 2011 March;63(1):21-34

Copyright © 2011 EDIZIONI MINERVA MEDICA

language: English

Desensitization and crossmatch conversion in deceased donor kidney transplantation

Bartel G., Böhmig G. A.

Division of Nephrology and Dialysis, Department of Medicine III, Medical University Vienna, Vienna, Austria


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Recipient allosensitization represents a major barrier to transplantation. Sensitized patients awaiting a deceased donor kidney transplant often face unacceptably long waiting times and are more prone to rejection, even in the absence of a positive crossmatch (XM). Two major strategies have been shown to facilitate the access to transplantation: specific allocation programs designed to enhance the availability of a well-matched allograft; and recipient desensitization to decrease levels of humoral alloreactivity. Over the last two to three decades, a variety of desensitization strategies have been published. Such protocols are based on the use of apheresis for direct alloantibody removal from the circulation, or high dose intravenous immunoglobulin and/or CD20 antibody rituximab for modulation of B cell immunity. An attractive approach may be the application of apheresis for rapid desensitization, with or without XM conversion, immediately before transplantation, a particular challenge because of the short interval between the transplant offer and surgery. It was shown that with currently available treatment strategies many high risk patients can be successfully transplanted within an acceptable time period. However, there is still a need for further improvement, as rejection and graft loss rates may be considerably higher than those documented for non-sensitized patients. Future studies will have to establish more precise diagnostic criteria to optimize treatment allocation and monitoring. Moreover, systematic trials are needed to assess the efficiency of innovative treatment concepts, such as the use of agents that directly affect alloantibody-producing plasma cells.

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georg.boehmig@meduniwien.ac.at