Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/39529
Title: De novo thrombotic microangiopathy following simultaneous pancreas and kidney transplantation managed with eculizumab.
Authors: Shochet L.;Mulley W. ;Ta J.;Kanellis J.;Simpson I.
Monash Health Department(s): Pathology
Nephrology
Institution: (Shochet, Kanellis, Mulley) Department of Nephrology, Monash Health, Melbourne, VIC, Australia (Simpson) Department of Anatomical Pathology, Monash Health, Melbourne, VIC, Australia (Kanellis, Mulley) Department of Medicine, Monash University, Melbourne, VIC, Australia (Ta) Australian Red Cross Blood Service, Melbourne, VIC, Australia
Issue Date: 13-Mar-2017
Copyright year: 2017
Publisher: Blackwell Publishing (E-mail: info@asia.blackpublishing.com.au)
Place of publication: Australia
Publication information: Nephrology. 22 (Supplement 1) (pp 23-27), 2017. Date of Publication: 01 Feb 2017.
Journal: Nephrology
Abstract: Thrombotic microangiopathy (TMA) is a well-recognised complication following transplantation, often due to an underlying genetic predisposition, medications or rejection. The use of eculizumab in these settings has been previously described, but its role still remains to be clarified. A 45-year-old man, with a history of type 1 diabetes mellitus and subsequent end-stage kidney failure, presented for a simultaneous pancreas-kidney transplant. Immunologically, he was well matched with the donor, and he received standard induction immunosuppression including tacrolimus. His early transplant course was complicated by Haemophilus parainfluenzae paronychia and a Pseudomonas aeruginosa catheter-associated urinary tract infection. Within 1 week, he developed thrombotic microangiopathy with significant renal dysfunction and eventual dialysis dependence, without evidence of transplant rejection on biopsy. He was also noted to have antiphospholipid antibodies in moderate titres. The TMA did not resolve despite cessation of tacrolimus, and he was subsequently commenced on eculizumab. The patient achieved a partial remission from TMA, with ongoing biochemical evidence of haemolysis, although now with stable graft function, despite significant damage. His transplanted pancreas remained seemingly unaffected by TMA, and continues to function well. This case describes an unusual presentation of TMA post-transplantation and is the only described case of eculizumab use following pancreas-kidney transplant. It remains unclear in this case what the likely precipitant for TMA was, although it seems to be, at least in part, controlled by ongoing use of eculizumab, presumably by terminal complement inhibition.Copyright © 2017 Asian Pacific Society of Nephrology
DOI: http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1111/nep.12936
PubMed URL: 28176480 [http://www.ncbi.nlm.nih.gov/pubmed/?term=28176480]
ISSN: 1320-5358
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/39529
Type: Review
Type of Clinical Study or Trial: Case series or case report
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