Plasmapheresis in transplantation

Despite all the advances in modern transplantation still remains the problem of acute or chronic rejection of transplanted organs. These processes have many reasons which can not always be eliminated. 

In cases coming transplantation without removing the remaining autoantibodies in the body, the transplanted kidney is at risk of the same autoimmune destruction as remote. On the other hand, the removal of the affected kidney with "pseudo-heterogenous" antigenic structure that encourages the constant reproduction of autoantibodies may contribute to remission and this pathological process [1]. 

Immune conflict after kidney transplantation may be the result of the emergence of anti-HLA antibodies as a result of isoimmunization in connection with previous transplants, blood transfusions or pregnancy. Despite the crossmatch with the donor organ, the presence of such HLA-antibodies leads to early rejection. Growth of donor-specific alloantibodies occurs within the first few weeks [2]. In some cases, under the influence of natural autoantibodies of IgG and IgM isotypes of complement system activation and endothelial cells can develop hyperacute rejection reaction in the next hours or even minutes [3]. 

Recurrence of focal segmental glomerulosclerosis in the transplanted kidney is observed in 30-80% of cases and deaths transplant within three years and up to 90% and only systematic conventional or cascade plasmapheresis after surgery prevents such complication [2, 4, 5, 6, 7]. Sometimes it takes a weekly plasmapheresis for nearly four years [8, 9, 10]. 

In cases with prolonged growing hypoproteinemia plasma exchange rates move to immuno-adsorption [11]. When combined taking courses plasmapheresis with rituximab (antilymphocyte immunoglobulin) or bortezomib achieved a longer remission of proteinuria [12, 13]. Nevertheless, we must bear in mind that rituximab itself can lead to serious complications that have to neutralize as by plasmapheresis [14]. 

R.M. Higgins et al. (1996), 9 patients had an immuno-adsorption before transplantation, which improved results and prognosis, even in cases where the previous rejection of transplanted kidneys. However M.D.Stegall et al. [15] believed that repeated sessions of plasmapheresis more reliably prevent rejection of the transplanted kidney than high doses of immunoglobulins. High frequency of graft rejection with hemolytic-uremic syndrome also requires prior course of plasmapheresis with ekulizumab [16]. 

Significant problems arise when forced kidney transplant under the ABO incompatibility. One reason is the presence of antigens A or B not only on the membranes of erythrocytes, but also on the walls of blood vessels, including transplanted kidney [17]. In this case, the recipients antibody (α or β) begin to interact with the antigens on the vascular wall, leading to disturbances of the microcirculation, and subsequent rejection of the transplanted organ ("large incompatibility"). "Shallow incompatibility" occurs as a result of generation of donor lymphocytes remaining in the transplanted organ as a "passenger", against the recipient erythrocytes, causing hemolysis of [18]. 

In these cases, a preliminary removal of anti-A or anti-B antibodies by plasma exchange substantially reduces the concentration of these antibodies, thereby smoothing rejection [19, 20, 21]. In cases of organ transplantation upcoming family donors, ABO incompatible, A.A. Ragimov et al. [22] performed courses of plasmapheresis to reduce the titer of antibodies to the respective levels of 1:2 - 1:4.In the case of the initial antibody titer 1:32 had to be removed to 350-550% CPV and repeated cases rise in antibody titer to 1:32 in the post-transplant period had again resorted to plasmapheresis with removal of up to 400% CPV. A.A.Tobian et al. (23) also reported the important role of plasmapheresis course, both before and after kidney transplantation with ABO-incompatibility, which eliminates episodes overactive antibody-dependent allograft rejection. Moreover, during the year the transplanted kidney proved viable in 100% of cases. Positive results were obtained when using the course immunoadsorption using columns Adsopak ABO-A production NPF POKARD [24].  

When liver transplant under the ABO incompatibility plasmapheresis was also used before surgery [25] and T. Ashizawa et al. [26] – both before and after surgery. Shimoda M. et al. [27] reported that preoperative administration of rituximab alone (without plasmapheresis) was unable to block the production of antibodies. Plasmapheresis should be used immediately, as soon as the first signs of organ rejection [28]. 
The same problems with ABO incompatibility arise in hematopoietic stem cell transplantation in oncology and a course of plasmapheresis before transplantation largely prevents rejection crises [29]. 

When transplanting organ to blood incompatibility ABO system has been used successfully also cascade plasmapheresis [30, 31]. At the same time, for 3-4 sessions cascade plasmapheresis managed to reduce the titer of anti-ABO antibodies to a concentration of 1:32, which is quite acceptable criterion for subsequent kidney transplantation in ABO incompatibility. 
It was possible to significantly (80-90%) reduce the content of group antibodies and using 3-4-selective immunoadsorption sessions using columns Ig-Adsopak for IgG-apheresis made ​​NPF POKARD in Russia [32]. 

After transplantation, a new situation – of the transplanted kidney comes antigenic signal, in response to which begin to form new antibodies with peak acute "crisis of rejection" in 1-2 weeks. And here efferent therapy can smooth these immune responses at lower levels of immunosuppressive therapy. The courses of plasmapheresis in such cases helps to restore urine output, decrease in serum creatinine and a gradual recovery of graft function, that 60% of patients allowed avoid "transplant-ectomy" [33]. 

In recent years, steel plasmapheresis spend even intraoperatively immediately after inclusion the transplanted kidney to blood flow, because it was found that major levels of proinflammatory cytokines (IL-6 , IL-8 , IL-10), the middle molecular weight toxins, and the lipid peroxidation products increases and reaches maximum by the end of the operation [34]. In addition to reducing the blood levels of endotoxin, the initial recovery of nitrogen and excretory renal function occurred significantly faster – to 5 - 6th day instead of 12-18 days in cases without the use of plasmapheresis [35]. Immunosuppressive therapy with plasmapheresis is able to block rejection reaction after transplantation also loops of the small intestine [36].

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