Imperial College London
Portrait Picture

DrCandiceRoufosse

Faculty of Medicine, Department of Immunology and Inflammation

Clinical Reader in Renal Pathology
 
 
 
//

Contact

 

+44 (0)20 3313 3280c.roufosse

 
 
//

Location

 

Commonwealth BuildingHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Broecker:2019:10.1111/his.13855,
author = {Broecker, V and Bardsley, V and Torpey, N and Perera, R and Montero, R and Dorling, A and Bentall, A and Neil, D and Willicombe, M and Berry, M and Roufosse, C},
doi = {10.1111/his.13855},
journal = {Histopathology},
pages = {88--103},
title = {Clinical-pathological correlations in post-transplant thrombotic microangiopathy},
url = {http://dx.doi.org/10.1111/his.13855},
volume = {75},
year = {2019}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - AimsPosttransplant thrombotic microangiopathy (TMA) is a rare and clinically challenging finding in renal transplant biopsies. In addition to recurrent atypical haemolytic uraemic syndrome, TMA in renal transplants is associated with various conditions, such as calcineurin inhibitor (CNI) treatment, antibodymediated rejection (ABMR), viral infections, sepsis, pregnancy, malignancies, and surgery. The therapeutic implications of this diagnosis are considerable. In order to better understand posttransplant TMA and to identify histological or clinical differences between associated causes, we conducted a multicentre retrospective study.Methods and resultsClinical parameters and transplant renal biopsy findings from 81 patients with TMA were analysed. Biopsies from 38 patients were also analysed with electron microscopy. On the basis of clinical–pathological correlation, TMA was attributed to a main aetiology, whenever possible. TMA occurred at a median of 30 days posttransplantation. Systemic features of TMA were present in only 18% of cases. Twentytwo per cent 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. The detection of ultrastructural features that are usually associated with ABMR may help to establish ABMR as the cause of TMA.ConclusionsAlthough CNI and ABMR appear to be the main contributors to posttransplant TMA, the aetiology of most cases is probably multifactorial, and TMA cannot be unequivocally attributed to a single underlying aetiology. Morphological features of TMA are not discriminating, but electron microscopy may help to identify ABMRassociated TMA.
AU  - Broecker,V
AU  - Bardsley,V
AU  - Torpey,N
AU  - Perera,R
AU  - Montero,R
AU  - Dorling,A
AU  - Bentall,A
AU  - Neil,D
AU  - Willicombe,M
AU  - Berry,M
AU  - Roufosse,C
DO  - 10.1111/his.13855
EP  - 103
PY  - 2019///
SN  - 0309-0167
SP  - 88
TI  - Clinical-pathological correlations in post-transplant thrombotic microangiopathy
T2  - Histopathology
UR  - http://dx.doi.org/10.1111/his.13855
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000472656400009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://onlinelibrary.wiley.com/doi/full/10.1111/his.13855
VL  - 75
ER  -
Download