Overlapping Pathways to Transplant Glomerulopathy: Chronic Humoral Rejection, Hepatitis C Infection and Thrombotic Microangiopathy

Détails

ID Serval
serval:BIB_EA0FCE644200
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Sous-type
Abstract (résumé de présentation): article court qui reprend les éléments essentiels présentés à l'occasion d'une conférence scientifique dans un poster ou lors d'une intervention orale.
Collection
Publications
Titre
Overlapping Pathways to Transplant Glomerulopathy: Chronic Humoral Rejection, Hepatitis C Infection and Thrombotic Microangiopathy
Titre de la conférence
ATC 2011, American Transplant Congress
Auteur(s)
Baid-Agrawal S., Farris A.B., Pascual M., Mauiyyedi S., Farrell M.L., Tolkoff-Rubin N., Collins A.B., Colvin R.B.
Adresse
Philadelphia, United-States, April 30-May 4, 2011
ISBN
1600-6135
Statut éditorial
Publié
Date de publication
2011
Volume
11
Série
American Journal of Transplantation
Pages
401
Langue
anglais
Notes
Publication type : Meeting Abstract
Résumé
Background:Transplant glomerulopathy (TG) has received much attention in recent years as a manifestation of chronic humoral rejection (CHR). However, many cases lack C4d deposition and/or circulating donor-specifi c antibodies, and the contribution of other potential causes has not been fully addressed.Methods: Of 209 consecutive renal allograft indication biopsies performed for chronic allograft dysfunction, 25 that met pathologic criteria of TG (>10% duplication of the GBM without immune complex deposition) were examined for various etiologies, including hepatitis C infection (HCV), thrombotic microangiopathy (TMA), and CHR. 29 cases of biopsy-proven isolated chronic calcineurin inhibitor toxicity from the same time period were used as controls for comparing the prevalence of HCV.Results: Three partially overlapping categories accounted for 84% of the cases: C4d+TG (48%), HCV+TG (36%) and TMA+TG (32%). The majority of TMA+ cases were HCV+ (63%) and the majority of HCV+ cases had TMA (56%). Donor specifi c antibodies were associated with C4d+TG (7/8 vs. 1/4 C4d-TG; P<0.02), but not with HCV+TG. The prevalence of HCV was higher in the TG group than in 29 control patients without TG (36% vs. 7%, P<0.01). HCV+TG patients developed allograft failure earlier than HCV-TG patients (67.2 ± 60.2 mo versus 153.4 ± 126.2 mo, P=0.02). On a multivariate analysis, out of HCV, TG and C4d, only HCV was found to be a signifi cant risk factor for a more rapid allograft loss.Conclusion: We conclude that TG is not a specifi c diagnosis, but a pattern of pathologic injury with 3 major overlapping pathways involving CHR, HCV infection and TMA. It is important to distinguish these mechanisms, as they may have differentprognostic and therapeutic implications.
Mots-clé
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Web of science
Création de la notice
13/05/2011 10:23
Dernière modification de la notice
20/08/2019 16:12
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