Date: Monday, June 4, 2018
Session Time: 4:30pm-6:00pm
Presentation Time: 5:42pm-5:54pm
Location: Room 6C
Thrombotic microangiopathy (TMA), whether de novo or recurrent, is a serious complication after renal transplantation, but prognostic factors and the role of complement inhibitors in the therapeutic strategy regarding de novo TMA are yet to be determined.
We retrospectively included all the patients with histopathologic lesions of TMA on for cause and/or screening kidney allograft biopsies performed between January 2004 and March 2016 in our center. The aims of our study were the description of clinicopathologic features and the identification of prognostic factors of de novo TMA.
98 patients experienced at least one episode of histological TMA, among which 90 % were de novo, (4,8% of the total kidney transplant population in our center). The median time of occurrence was 198±920 days. The majority (83,7%) of cases were TMA localized in the graft. The etiological factors were multiple in more than one-third of cases, antibody-mediated rejection being the most frequent cause (46,9%), whereas underlying abnormalities of the alternative complement pathway were proved or suspected in 10,2 % of de novo TMA, even in localized forms. Graft survival was worst compared to kidney transplant recipients without TMA (84.7% vs 91.3% after 5 years respectively ; p<0.0001). The rate of graft loss after one year among patients with de novo TMA and recurrent TMA was 8 % and 10% respectively. The 2 main factors associated with graft loss were score of intimal arteritis and renal function at the time of diagnosis. The histological pattern of TMA was not discriminative of any etiology, even if arteriolar pattern and glomerular pattern were more often associated with calcineurin-inhibitor toxicity and antibody-mediated rejection respectively.
These results confirm the theory of the " multiple hit " with often multiple causal factors and the implication of alternative complement pathway dysregulation in the pathogenesis of some cases of de novo TMA. It also underlines the prognostic value of histology but its current limits to provide the clinician with etiologic clues.
CITATION INFORMATION: Dessaix K., Bontoux C., Aubert O., Zuber J., Sberro Soussan R., Frémeaux-Bacchi V., Le Quintrec M., Legendre C., Rabant M. Thrombotic Microangiopathy after Renal Transplantation: A Clinicopathological Study and Identification of Prognostic Factors Am J Transplant. 2017;17 (suppl 3).
To cite this abstract in AMA style:Dessaix K, Bontoux C, Aubert O, Zuber J, Soussan RSberro, Frémeaux-Bacchi V, Quintrec MLe, Legendre C, Rabant M. Thrombotic Microangiopathy after Renal Transplantation: A Clinicopathological Study and Identification of Prognostic Factors [abstract]. https://atcmeetingabstracts.com/abstract/thrombotic-microangiopathy-after-renal-transplantation-a-clinicopathological-study-and-identification-of-prognostic-factors/. Accessed June 15, 2021.
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