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JOURNAL ARTICLE

Clinical-pathological Correlations in Post-Transplant Thrombotic Microangiopathy

Verena Broecker, Victoria Bardsley, Nicholas Torpey, Ranmith Perera, Rosa Montero, Anthony Dorling, Andrew Bentall, Desley Neil, Michelle Willicombe, Miriam Berry, Candice Roufosse
Histopathology 2019 March 9
30851188

AIMS: Post-transplant thrombotic microangiopathy (TMA) is a rare and clinically challenging finding in renal transplant biopsies. In addition to recurrent atypical haemolytic uremic syndrome (aHUS), TMA in renal transplants is associated with various conditions, such as calcineurin-inhibitor (CNI) treatment, antibody-mediated rejection (ABMR), viral infections, sepsis, pregnancy, malignancies or surgery. The therapeutic implications of this diagnosis are considerable. In order to better understand post-transplant TMA and to identify histological or clinical differences between associated causes, we conducted a multi-centre retrospective study.

METHODS AND RESULTS: Clinical parameters and transplant renal biopsy findings from 81 patients with TMA were analysed. Biopsies from 38 patients were also analysed by electron microscopy. Based on clinical-pathological correlation, TMA was attributed to a main aetiology, whenever possible. TMA occurred at a median of 30 days post-transplantation. Systemic features of TMA were present in only 18%. 22% of cases were attributed to CNI and 11% to ABMR. Although other potentially contributing factors were found in 56% of patients, in most cases (63%) no clearly attributable cause of TMA was identified. Histological differences between groups were minimal. Detection of ultrastructural features usually associated with ABMR may help establish ABMR as the cause of TMA.

CONCLUSIONS: Although CNI and ABMR appear to be the main contributors to post-transplant TMA, aetiology of most cases is likely multifactorial and TMA cannot be unequivocally attributed to a single underlying aetiology. Morphological features of TMA are not discriminating but electron microscopy may help identify ABMR-associated TMA. This article is protected by copyright. All rights reserved.

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