Use of Eculizumab for Active Antibody-mediated Rejection That Occurs Early Post-kidney Transplantation: A Consecutive Series of 15 Cases.
Adult
Allografts
Antibodies, Monoclonal, Humanized
/ therapeutic use
Biopsy
Complement Inactivating Agents
/ therapeutic use
Female
Flow Cytometry
Graft Rejection
/ drug therapy
Graft Survival
Humans
Immunosuppression Therapy
Isoantibodies
/ immunology
Kidney Failure, Chronic
/ surgery
Kidney Transplantation
Male
Middle Aged
Postoperative Complications
Retrospective Studies
Treatment Outcome
Journal
Transplantation
ISSN: 1534-6080
Titre abrégé: Transplantation
Pays: United States
ID NLM: 0132144
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
pubmed:
26
2
2019
medline:
23
6
2020
entrez:
26
2
2019
Statut:
ppublish
Résumé
Active antibody-mediated rejection (AMR) that occurs during the amnestic response within the first month posttransplant is a rare but devastating cause of early allograft loss after kidney transplant. Prior reports of eculizumab treatment for AMR have been in heterogeneous patient groups needing salvage therapy or presenting at varied time points. We investigated the role of eculizumab as primary therapy for active AMR early posttransplant. We performed a retrospective observational study of a consecutive cohort of solitary kidney transplant recipients who were transplanted between January 1, 2014, and January 31, 2018, and had AMR within the first 30 days posttransplant and treated with eculizumab ± plasmapheresis. Fifteen patients had early active AMR at a median (interquartile range [IQR]) of 10 (7-11) days posttransplant and were treated with eculizumab ± plasmapheresis. Thirteen cases were biopsy proven, and 2 cases were presumed on the basis of donor-specific antibody trends and allograft function. Within 1 week of treatment, the median estimated glomerular filtration rate increased from 21 to 34 mL/min (P = 0.001); and persistent active AMR was only found in 16.7% (2/12) of biopsied patients within 4-6 months. No graft losses occurred, and at last follow-up (median [IQR] of 13 [12-19] mo), the median IQR estimated glomerular filtration rate increased to 52 (46-60) mL/min. Prompt eculizumab treatment as primary therapy is safe and effective for early active AMR after kidney transplant or abrupt increases in donor-specific antibodies when biopsy cannot be performed for diagnosis confirmation.
Sections du résumé
BACKGROUND
Active antibody-mediated rejection (AMR) that occurs during the amnestic response within the first month posttransplant is a rare but devastating cause of early allograft loss after kidney transplant. Prior reports of eculizumab treatment for AMR have been in heterogeneous patient groups needing salvage therapy or presenting at varied time points. We investigated the role of eculizumab as primary therapy for active AMR early posttransplant.
METHODS
We performed a retrospective observational study of a consecutive cohort of solitary kidney transplant recipients who were transplanted between January 1, 2014, and January 31, 2018, and had AMR within the first 30 days posttransplant and treated with eculizumab ± plasmapheresis.
RESULTS
Fifteen patients had early active AMR at a median (interquartile range [IQR]) of 10 (7-11) days posttransplant and were treated with eculizumab ± plasmapheresis. Thirteen cases were biopsy proven, and 2 cases were presumed on the basis of donor-specific antibody trends and allograft function. Within 1 week of treatment, the median estimated glomerular filtration rate increased from 21 to 34 mL/min (P = 0.001); and persistent active AMR was only found in 16.7% (2/12) of biopsied patients within 4-6 months. No graft losses occurred, and at last follow-up (median [IQR] of 13 [12-19] mo), the median IQR estimated glomerular filtration rate increased to 52 (46-60) mL/min.
CONCLUSIONS
Prompt eculizumab treatment as primary therapy is safe and effective for early active AMR after kidney transplant or abrupt increases in donor-specific antibodies when biopsy cannot be performed for diagnosis confirmation.
Identifiants
pubmed: 30801549
doi: 10.1097/TP.0000000000002639
pmc: PMC6699919
mid: NIHMS1519153
doi:
Substances chimiques
Antibodies, Monoclonal, Humanized
0
Complement Inactivating Agents
0
Isoantibodies
0
eculizumab
A3ULP0F556
Types de publication
Journal Article
Observational Study
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2397-2404Subventions
Organisme : NCATS NIH HHS
ID : KL2 TR002379
Pays : United States
Commentaires et corrections
Type : CommentIn
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