scholarly journals De novo thrombotic microangiopathy following simultaneous pancreas and kidney transplantation managed with eculizumab

Nephrology ◽  
2017 ◽  
Vol 22 ◽  
pp. 23-27 ◽  
Author(s):  
Lani Shochet ◽  
John Kanellis ◽  
Ian Simpson ◽  
Joseph Ta ◽  
William Mulley
Keyword(s):  
Kidney Transplantation ◽  
Thrombotic Microangiopathy ◽  
De Novo

scholarly journals P1654INCIDENCE AND RISK FACTORS OF THROMBOTIC MICROANGIOPATHY AFTER KIDNEY TRANSPLANTATION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Kenta Futamura ◽  
Goto Norihiko ◽  
Hiroki Fukuhara ◽  
Takaaki Nawano ◽  
Akiko Kanda ◽  
...  
Keyword(s):  
Risk Factors ◽  
Kidney Transplantation ◽  
Graft Survival ◽  
Thrombotic Microangiopathy ◽  
De Novo ◽  
Pathological Findings ◽  
Post Transplant ◽  
Antibody Mediated Rejection ◽  
Abo Incompatibility ◽  
Biopsy Specimens

Abstract Background and Aims Thrombotic microangiopathy (TMA) is characterized by mechanical hemolytic anemia, thrombocytopenia, and renal impairment. TMA that occurs in kidney transplant recipients has multiple etiologies and may be de novo or recurrent. Main causes of TMA among recipients are atypical hemolytic uremic syndrome (aHUS), immunosuppressive drugs, ischemia-reperfusion injury (IRI), viral infections, and antibody-mediated rejection (ABMR). Pathological findings of TMA with thrombosis in glomeruli and arterioles are not rare in graft biopsies, but the clinical signs vary widely by etiologies, and incidence and risk factors for each are uncertain. The purpose of this study is to clarify the current status of TMA after kidney transplantation. Method The subjects were 1,336 patients (5,425 biopsy specimens) who underwent kidney transplantation (851 ABO-compatible and 485 ABO-incompatible) at Japanese Red Cross Nagoya Daini Hospital and Masuko Memorial Hospital from January 1, 2000 to June 30, 2018. We investigated patient characteristics and graft survival in 69 patients with pathological findings of TMA (12 with symptomatic TMA and 57 with asymptomatic TMA) and 1,207 patients without findings of TMA. Sixty patients were excluded because of incomplete data or biopsy specimens. TMA patients with acute kidney injury (AKI) were defined as symptomatic TMA in this study. Results The incidence of post-transplant TMA was 5.2% (symptomatic TMA : 0.9%, asymptomatic TMA : 4.3%) in our cohort. Multivariate analysis revealed significant risk factors for TMA were presence of donor specific antibodies (DSA) and use of cyclosporine (odds ratio [OR] 3.52; 95% confidence interval [CI] 1.58-7.88; p=0.002 and OR 3.70; 95% CI 1.68-8.11; p=0.001, respectively). Causes of symptomatic TMA were ABMR : 66.7% (5 patients with ABO-incompatibility, 3 with preformed DSA), aHUS : 16.7%, cytomegalovirus and adenovirus infection : 8.3%, and causes of asymptomatic TMA were drug-induced: 40.4% (21 patients with calcineurin inhibitor, 2 with everolimus), ABMR: 31.6% (10 with ABO-incompatibility, 8 with de novo DSA), IRI : 14.0 %. Onset of post-transplant TMA was significantly associated with lower graft survival (Figure A), with a stronger correlation in symptomatic TMA than in asymptomatic TMA (Figure B and C). Conclusion TMA with AKI that occurred after kidney transplantation had a poor graft prognosis. Therefore, avoiding transplantation, changing donors or using tacrolimus instead of cyclosporine should be considered for patients with DSA or ABO-incompatibility.

De novo thrombotic microangiopathy after kidney transplantation

2018 ◽  
Vol 32 (1) ◽  
pp. 58-68 ◽  
Author(s):  
Neetika Garg ◽  
Helmut G. Rennke ◽  
Martha Pavlakis ◽  
Kambiz Zandi-Nejad
Keyword(s):  
Kidney Transplantation ◽  
Thrombotic Microangiopathy ◽  
De Novo

Analysis of the prevalence of systemic de novo thrombotic microangiopathy after ABO ‐incompatible kidney transplantation and the associated risk factors

2019 ◽  
Vol 26 (12) ◽  
pp. 1128-1137 ◽  
Author(s):  
Masayuki Tasaki ◽  
Kazuhide Saito ◽  
Yuki Nakagawa ◽  
Naofumi Imai ◽  
Yumi Ito ◽  
...  
Keyword(s):  
Risk Factors ◽  
Kidney Transplantation ◽  
Thrombotic Microangiopathy ◽  
De Novo ◽  
Associated Risk Factors

Thrombotic microangiopathy after kidney transplantation: causes, clinical specifics and outcomes

2020 ◽  
Vol 48 (3) ◽  
pp. 177-186
Author(s):  
E. I. Prokopenko ◽  
E. O. Shcherbakova ◽  
R. O. Kantaria ◽  
V. A. Stepanov
Keyword(s):  
Kidney Transplantation ◽  
Renal Transplant ◽  
Graft Survival ◽  
Thrombotic Microangiopathy ◽  
De Novo ◽  
Renal Transplant Recipients ◽  
Post Transplant ◽  
Antibody Mediated Rejection ◽  
Renal Graft ◽  
Kidney Transplantations

Background: Thrombotic microangiopathy (TMA) is a clinical and morphological phenomenon characterized by specific microvascular injury, microangiopathic hemolytic anemia, and damage of various target organs. TMA after kidney transplantation (post-renal transplant TMA) is a serious complication affecting the recipient and graft survival.Aim: To analyze the timing, causes, specifics of the clinical course and outcomes of TMA in renal transplant recipients.Materials and methods: This one-center study was based on a comprehensive examination and follow-up of 697 patients who had undergone 728 kidney transplantations (KT) from deceased donors in 2003–2019. Post-transplant TMA of the renal graft was confirmed morphologically in all cases.Results: We identified 32 episodes of post-transplant TMA in 32 patients; thus, the incidence of TMA was 4.4%. All cases developed after KT de novo; no recurrent TMA was observed. TMA was systemic in 37.5% and locally renal in 62.5% of the patients. The median time to the development of post-transplant TMA was 0.55 (range, 0.1 to 51.6) months. The patients with TMA did not differ from those without by gender, age, body mass index, underlying disorders, type and duration of dialysis before KT, protocols of immunosuppressive therapy, incidence of surgical, urological, infectious, cardiovascular and oncological complications. The patients with TMA were significantly more likely to have graft rejection (25.0% vs 11.2%, p = 0.035) and a never-functioning transplant (28.1% vs 4.9%, p < 0.001). The presence of TMA negatively affected the transplantation outcomes. The cumulative 1-year graft survival in the patients without and with TMA was 91% and 44%, respectively, whereas their 5-year survival rates were 68% and 25% (p < 0.001). The leading causes of TMA were: donor pathology (31.2%), antibody-mediated rejection (28.1%), and cyclosporine/tacrolimus nephrotoxicity (21.9%); the proportion of other causes was 18.8%. A combination of TMA etiological factors was identified in 68.7% of the recipients. The recipients with of calcineurin inhibitors nephrotoxicity had a more favorable prognosis compared to those with other causes of TMA.Conclusion: Post-renal transplant TMA is an infrequent but serious complication that worsens the graft survival and often is life-threatening for recipients. In most cases, TMA develops in the early post-operative period; however, it can occur any time thereafter. To improve the outcome of TMA, early diagnosis is necessary based on clinical suspicion and a prompt biopsy of the renal graft with suspected TMA. Treatment should be started quickly with consideration of the cause of the complication.

scholarly journals De Novo and recurrent thrombotic microangiopathy (TMA) after renal transplantation: current concepts in management

2021 ◽  
Vol 9 (1) ◽  
pp. 23-30
Author(s):  
Fedaei Abbas ◽  
Sara Fedaei Abbas
Keyword(s):  
Kidney Transplantation ◽  
Thrombotic Microangiopathy ◽  
De Novo ◽  
Therapeutic Option ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Previous History ◽  
Therapeutic Interventions ◽  
Favorable Prognosis ◽  
Uremic Syndrome ◽  
The Cost

Thrombotic microangiopathy (TMA) is a well-recognized complication of kidney transplantation that leads frequently to allograft failure. This serious outcome depends greatly on the underlying etiology as well as the timing of therapeutic interventions. TMA syndromes may occur with no previous history of TMA, i.e., de novo TMA, mostly due to medications or infection, or more frequently recurs after kidney transplantation i.e., recurrent TMA in patients with ESRF due to the atypical hemolytic uremic syndrome (aHUS). On the other hand, patients with shiga-toxin induced HUS (classic HUS), particularly in childhood has a favorable prognosis. One of the fundamental tools of management of this disease is the genetic screening for abnormal mutations, determination of which will recognize the tools of therapy and consequently outcome of the disease to a large extent. While patients with CFH and CFI mutations have a worse prognosis, other patients with MCP mutations-for example- have a more favorable prognosis. Accordingly, plan of therapy can be thoroughly drawn with a better chance of cure. Unfortunately, the successful use of the biological agent “eculizumab”, an anti-C5 agent, in some of these syndromes is largely impeded by its high cost linked to its use as a life-long therapy. However, a new therapeutic option has been recently admitted ameliorating this drawback and improve the cost-effectiveness balance.

1949: Six Month Randomized Study Comparing Cyclosporine Microemulsion with C2 Monitoring and Tacrolimus in De Novo Kidney Transplantation

2004 ◽  
Vol 171 (4S) ◽  
pp. 515-515
Author(s):  
Felipe G. Balbontin ◽  
Bryce Kiberd ◽  
Philip Belitsky ◽  
Dharm Singh ◽  
Albert Fraser ◽  
...  
Keyword(s):  
Kidney Transplantation ◽  
De Novo ◽  
Randomized Study ◽  
C2 Monitoring ◽  
Cyclosporine Microemulsion
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