**6.2. Plasma exchange/plasmapheresis**

Plasma exchange removes antibodies from the circulation. In the case of ABMR it is thought to be efficacious through the removal of DSAs. However, it does not suppress further pro‐ duction. In fact, it may stimulate rebound immunoglobulin production if used on its own. It is hence necessary to use it in conjunction with strategies which target antibody production (for example, the anti-CD20 monoclonal antibody rituximab). ABMR treatment protocols may utilise plasma exchange depending upon the antibody titre, the affinity of the antibody for the antigen, the dose of IVIg and use of other agents.[42]

#### **6.3. Rituximab**

This is a humanised mouse monoclonal antibody that targets CD20, which is expressed on the majority of B cells. However, most plasma cells lack CD20 and are unaffected by Rituximab. Hence, its role will be as an adjunctive treatment. A recent single centre study compared outcomes in 24 cases of ABMR treated with either high dose IVIg (2g/kg for four doses) versus plasmapheresis plus IVIg (100mg/kg) for four treatments followed by IVIg (2g/kg for four doses) and two doses of rituximab (375mg/m2). Improved 3-year survival (92% vs. 50%) and significantly reduced DSA at 3 months was observed in the plasmapheresis/IVIg/rituximab group.[6] It has also been seen to be effective when used as part of desensitization protocol in ABO- incompatible (ABOI) transplants, although there is concern over the cost of increased infections in recipients of such transplants. One study reported \patients who received B-cell depletion with rituximab as an induction agent had significant reductions in DSA generation and rates of chronic transplant glomerulopathy over 5 years compared with ABO-compatible low-risk transplant recipients who did not receive rituximab.[50]
