Severe early acute humoral rejection resulting in allograft loss in a renal transplant recipient with Campath-1H induction therapy

Hill, Prue; Gagliardini, Elena; Ruggenenti, Piero

doi:10.1093/ndt/gfh867

Cited by 20 publications

(11 citation statements)

References 12 publications

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“…It has also been suggested that CD45RO ϩ memory T cells are incompletely depleted by alemtuzumab and may play a prominent role in the development of acute rejection after alemtuzumab induction (6). Additionally, there have been reports of acute humoral rejection occurring after alemtuzumab induction (12,23). This may potentially be mediated by B cells, which have been noted to repopulate to levels beyond baseline after depletion by alemtuzumab (6).…”

Section: Discussionmentioning

confidence: 99%

Alemtuzumab Induction in Deceased Donor Kidney Transplantation

et al. 2007

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Section: Discussionmentioning

confidence: 99%

Alemtuzumab Induction in Deceased Donor Kidney Transplantation

et al. 2007

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“…However, despite its reactivity against B cells, it has been unable to prevent and in fact may result in increased rates of C4d-positive, AMR when used without a calcineurin inhibitor (42)(43)(44). It also seems that memory T cells are resistant to alemtuzumab therapy (45,46).…”

Section: Other Approaches To Desensitizationmentioning

confidence: 99%

Presensitization

Jordan¹,

Pescovitz²

2006

Clinical Journal of the American Society of Nephrology

110

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Much attention has been placed recently on transplantation in highly HLA-sensitized patients. In attempts to remove these antibodies and enable successful transplantation, several novel approaches have been developed. These include intravenous Ig (IVIg), mycophenolate mofetil, sirolimus, alemtuzumab, protein A immunoabsorption, and rituximab. IVIg has emerged as a very effective agent when used alone in high dose or when used in low dose and combined with plasmapheresis. Although alemtuzumab has been used to eliminated B cells, it fails to prevent antibody-mediated rejection and therefore probably is not suitable for desensitization. Rituximab, a B cell-specific antibody, seems to be safe and to have some efficacy as a sole agent in elimination of alloantibodies but most likely will require combination therapy with IVIg or other agents. Newer agents, such as humanized anti-CD20, are being developed. Despite the great interest in the problem of allosensitization, with one notable exception, there is a major deficiency in controlled clinical trials, the conduct of which should be a focus for the near future.

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“…However, alemtuzumab treatment was associated with an increased risk for the development of donorspecific anti-HLA Abs (DSA) and with an excess risk for early Ab-mediated rejection, particularly in a calcineurin inhibitor-free immunosuppressive regimen (3)(4)(5). The above data converge to suggest that, in the clinical setting of minimal maintenance immunosuppression, alemtuzumab-induced lymphocyte depletion might result in activation of the humoral response toward alloantigens.…”

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confidence: 99%

In Kidney Transplant Patients, Alemtuzumab but Not Basiliximab/Low-Dose Rabbit Anti-Thymocyte Globulin Induces B Cell Depletion and Regeneration, Which Associates with a High Incidence of De Novo Donor-Specific Anti-HLA Antibody Development

Todeschini

Cortinovis

Perico

et al. 2013

The Journal of Immunology

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In this single-center matched-cohort study, we evaluated the phenotype of repopulating B cells and its correlation with donor-specific anti-HLA Ab development and long-term graft function in 16 renal transplant recipients and 32 age- and gender-matched controls induced with alemtuzumab or basiliximab (Bas)/low-dose rabbit anti-thymocyte globulin (rATG), respectively. Alemtuzumab, but not Bas/rATG, profoundly depleted peripheral B cells in the first 2 mo posttransplantation. Early posttransplant, naive B cells were significantly depleted, whereas Ag-experienced and memory B cells were partially spared. Transitional B cells transiently increased 2 mo posttransplant. At month 6 posttransplant, pregerminal center B cells emerged, a process promoted by increased BAFF serum levels. Thereafter, B cell counts increased progressively, mainly due to expansion of naive B cells. Conversely, Bas/rATG did not modify the B cell phenotype throughout the follow-up period. Alemtuzumab was associated with a higher incidence of de novo DSA compared with Bas/rATG. DSA development was predicted by changes in the B cell compartment and correlated with worse long-term graft function. Thus, alemtuzumab-induced B cell depletion/reconstitution may promote chronic humoral responses against the graft.

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Severe early acute humoral rejection resulting in allograft loss in a renal transplant recipient with Campath-1H induction therapy

Cited by 20 publications

References 12 publications

Alemtuzumab Induction in Deceased Donor Kidney Transplantation

Alemtuzumab Induction in Deceased Donor Kidney Transplantation

Presensitization

In Kidney Transplant Patients, Alemtuzumab but Not Basiliximab/Low-Dose Rabbit Anti-Thymocyte Globulin Induces B Cell Depletion and Regeneration, Which Associates with a High Incidence of De Novo Donor-Specific Anti-HLA Antibody Development

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